COLLEGE  OF   OSTEOPATHIC   PHYSICIANS 
AND  SURGEONS   •  LOS  ANGELES,  CALIFORNIA 


E  c  T 


ON 


DISEASES 


RESPIRATORY    ORGANS, 


HEART    AND   KIDNEYS. 


V 


ALFRED   L.  LOOMIS,  M.D., 

PROFESSOR    OF    PATHOLOGY  AND   PRACTICAL    MEDICINE    IN    THE    MEDICAL    DEPARTMENT  OJP  TUB 
UNIVERSITY  OP  TUB  CITY  OP    NEW    YORK ;    CONSULTING    PHYSICIAN    TO   THE  CHARITY 
HOSPITAL,  TO  THE  BUREAU  OP  OUT-DOOR  RELIEF,  TO  THE  CENTRAL  DISPEN- 
SARY ;    VISITING  PHYSICIAN  TO  THE  BELLEVUE  HOSPITAL,  TO  THE 
MOUNT  SINAI   HOSPITAL,    ETC.,  ETC. 


NEW    YORK: 

WILLIAM    WOOD     &     COMPANY, 

27  GREAT  JONES  STREET. 

1876. 


X     i^ 


Entered  according  to  Act  ot  Congress,  in  the  year  1875,  by 

WILLIAM  WOOD   &  CO., 
In  the  Office  of  the  Librarian  of  Congress  at  Washington. 


JOHN  F.  TROW  &  SON, 

STEREOTYPERS  AND  PRINTERS, 

205—213  East  i2//z  Street, 

NEW    YORK. 


&o  tl)e 

ALUMNI    AND    STUDENTS 

OF    THK 

MEDICAL  DEPARTMENT  OF  THE  UNIVERSITY  OF  THE  CITY  OF  NEW  YORK, 

THESE   LECTURES   ARE   DEDICATED 

BY  THEIR  SINCERE  FRIEND, 

THE   AUTHOR. 


PREFACE. 


THESE  Lectures  were  delivered  in  the  Medical  Department 
of  the  University  of  the  City  of  New  York  to  the  class  of 
1874.  With  unimportant  alterations,  I  offer  them  as  they 
were  phonographically  reported  by  Dr.  W.  M.  Carpenter. 

I  am  confident  that  the  stimulus  of  the  lecture-room  has 
made  prominent  many  practical  points  which  would  have 
been  passed  over,  had  I  attempted  a  complete  and  sys- 
tematic treatise  upon  the  subjects  under  consideration. 

In  their  preparation  my  custom  has  been,  after  careful 
reading  and  a  close  analysis  of  the  subject  of  each  lecture, 
to  trust  that  the  stimulus  of  tfte  class  would  enable  me  to 
present  the  most  recent  views  of  acknowledged  authorities, 
combined  with  the  results  of  my  own  clinical  observation 
and  experience,  in  so  simple,  intelligible,  and  concise  a 
form,  that  each  student  might  fully  master  its  prominent 
points. 

I  have  endeavored  to  avoid,  as  far  as  possible,  all  doubt- 
ful and  disputed  points,  and  have  referred  to  theoretical 
questions  only  so  far  as  they  seemed  to  me  to  throw  light 
upon  the  etiology,  pathology,  diagnosis,  and  treatment  of 
the  different  forms  of  disease  which  I  have  considered. 

It  is  my  purpose,  at  some  future  time,  to  publish,  in 
a  similar  form,  lectures  upon  other  important  subjects 
connected  with  Practical  Medicine. 

42  WEST  25TH  STREET,  NEW  YORK, 
February,  1875. 


CONTENTS. 


LECTUKE  I. 

DISEASES  OF  THE  LARYNX. 

PAGE 

Acute  Catarrhal  Laryngitis — Chronic  Gatarrhal  Laryngitis — (Edema  Glottidis      1 

LECTURE   II. 

DISEASES  OP  THE  LARYNX 

Acute  Croupous  Laryngitis  (Membranous  Croup) — Ulcers  of  the  Larynx. ...     15 

LECTURE   III. 

DISEASES  OP  THE  LARYNX. 

Laryngeal    Paralysis — Spasmodic    Affections  of  the   Larynx — Pathological 

New  Formations  in  the  Larynx » 27 

LECTURE    IV. 
BRONCHITIS. 

Definition — Acute  Catarrhal    Bronchitis    of    the    larger    Tubes — Capillary 

Bronchitis 40 

LECTURE   V. 
BRONCHITIS. 

Chronic  Catarrhal  Bronchitis — Bronchial  Dilatation — Croupous  Bronchitis. .     52 

LECTURE  VI. 

ASTHMA. 
Spasmodic  Asthma — Hay- Asthma — Whooping-cough 66 

LECTURE   VII. 

PULMONARY  EMPHYSEMA. 

Vesicular  Emphysema — Interlobular  Emphysema 79 


vm  CONTENTS. 

LECTURE 


PULMONARY  CEDEMA. 

PAGB 

Pulmonary  Congestion  —  Pulmonary  Apoplexy  ...........................     93 

LECTURE   IX. 

BRONCHIAL  HEMORRHAGE. 

Gangrene  of  the  Lungs  —  Cancer  of  the  Lungs  ............................  108 

LECTURE   X. 
PNEUMONIA. 

Varieties  —  Croupous  or  Lobar  Pneumonia  ................................  120 

LECTURE  XL 

PNEUMONIA. 

Croupous  or  Lobar  Pneumonia  (continued)  ...............................  132 

LECTURE  XII. 

PNEUMONIA. 

Croupous  or  Lobar  Pneumonia  (continued)  —  Catarrhal  or  Lobular  Pneumo- 

nia ..........................................................  143 

LECTURE  XIII. 

PNEUMONIA. 
Acute  Catarrhal  Pneumonia  (continued)  —  Interstitial  Pneumonia  ..........   155 

LECTURE  XIV. 

PLEURISY. 

Definition  —  Varieties  —  Acute  Pleurisy  ...................................  169 

LECTURE  XV. 
PLEURISY. 

Subacute  Pleurisy  .....................................................  180 

LECTURE  XVI. 

PLEURISY. 

Subacute  Pleurisy  (continued)  —  Chronic  Pleurisy  .........................  190 


CONTENTS.  IX 

LECTUEE  XVII. 

PLEURISY. 

PAOE 

Chronic  Pleurisy  (contirraed) — Hydropneumothorax.  — Hydrothorax.  — Hsera- 

athorax 202 

LECTURE  XVIII. 
PULMONARY  PHTHISIS. 

Catarrhal  Phthisis — Morbid  Anatomy — Fibrous  Phthisis — Morbid  Anatomy 

— Tubercular  Phthisis — Morbid  Anatomy 213 

LECTURE  XIX. 

PULMONARY  PHTHISIS. 

Etiology  of  the  Different  Varieties 226 

LECTURE  XX. 

PULMONARY  PHTHISIS. 
Symptoms  common  to  all  Varieties 238 

LECTURE  XXI. 

PULMONARY  PHTHISIS. 

Physical  Signs — Differential  Diagnosis 250 

LECTURE  XXII. 

PULMONARY  PHTHISIS. 

Prognosis — Treatment 261 

LECTURE  XXIII. 

PULMONARY  PHTHISIS. 

Treatment  (continued) 273 

LECTURE  XXIV. 

DISEASES   OF   THE   HEART. 

Different  Forms — Acute  Pericarditis 287 

LECTURE  XXV. 

ACUTE   PERICARDITIS. 

Chronic  Pericarditis — Hydropericardium — Pneumopericardium — Hsemoperi- 

cardiutn — Tubercles  of  the  Pericardium . .  .  298 


X  CONTEXTS. 

LECTURE  XXVI. 

ENDOCARDITIS. 

PAGE 

Acute  Endocarditis — TJlcerative  Endocarditis 309 

LECTURE  XXVII. 

CHRONIC   ENDOCARDITIS. 

Valvular  Murmurs  and  their   relation  to  Valvular  Diseases — Aortic   Ob- 
struction   320 

LECTURE  XVIII. 

VALVULAR  LESIONS. 
Aortic  Obstruction — Aortic  Regurgitation 330 

LECTURE  XXIX. 

VALVULAR  DISEASES. 

Aortic  Regurgitation — Mitral  Obstruction — Mitral  Regnrgitation 340 

LECTURE  XXX. 

VALVULAR  DISEASES. 

Mitral  Regurgitation — Valvular  Diseases  of    the  Right   Heart — Pulmonic 

Obstruction — Pulmonic  Regurgitation 351 

LECTURE  XXXT. 
VALVULAR  DISEASES  AND  VALVULAR  MURMURS. 

Tricuspid  Stenosis — Tricuspid   Regurgitation — Diagnosis  of    Cardiac  Mur- 
murs   363 

LECTURE  XXXII. 
CARDIAC  HYPERTROPHY. 

Definition — Varieties 376 

LECTURE  XXXIII. 
CAKDIAC  DILATATION. 

Definition — Varieties 388 

LECTURE  XXXIV. 

CARDIAC  DEGENERATION. 

Myocarditis — Fatty  Degeneration  of  the  Heart. . . 401 


CONTENTS.  XI 

LECTURE  XXXV. 

CARDIAC   DEGENERATIONS. 

PAGE 

Amyloid  Degeneration — Muscular  Atrophy — Rupture  of  the  Heart — Aneu- 
risms of  the  Heart — Cardiac  Thrombosis — New  Formations  in  the 
Heart — Neuroses  of  the  Heart 413 

LECTURE  XXXVI. 

DISEASES  OP   THE   KIDNEYS. 

Introduction — Renal  Congestion — Renal  Hemorrhage 431 

LECTURE  XXXVII. 

ACUTE   URAEMIA. 

Ursemic  Convulsions — Uraemic  Coma 442 

LECTURE  XXXVIII. 
BRIGHT'S  DISEASES  OF  THE  KIDNEY. 

Definition  of  the  Term — Parenchymatous  Nephritis  (Morbid  Anatomy) — 

Amyloid  Degeneration  of  the  Kidneys  (Morbid  Anatomy) 453 

LECTURE  XXXIX. 
BRIGHT'S  DISEASES. 

Cirrhotic  or  Gouty  Form  (Morbid  Anatomy) — Parenchymatous  Nephritis — 

(Etiolog/  and  Symptoms) 465 

LECTURE   XL. 

BRIGHT'S  DISEASES. 

Parenchymatous  Nephritis — Symptoms 476 

LECTURE  XLI. 
BRIGHT'S  DISEASES. 

Parenchymatous  Nephritis  (continued) — Differential  Diagnosis — Amyloid 
Degeneration  of  Kidneys  ;  Etiology,  etc.— Cirrhotic  Kidney  ;  Etiol- 
ogy, etc 487 

LECTURE    XLII. 

BRIGHT'S  DISEASES. 

Cirrhotic  Kidney— Symptoms,  etc .• 499 


Xii  CONTENTS. 

LECTURE  XLIII. 
BRIGHT'S  DISEASES. 

PAGE 

Treatment  (continued) 509 

LECTURE  XLIV. 

PYELITIS. 

Pyonephrosis — Hydronephrosis — Cystic    Kidney — Renal   Concretions — New 

Growths  in  the  Kidney 520 


DISEASES    OF   THE   RESPIBA- 
TOKY   ORGANS. 


LECTURE    I. 


DISEASES  OF  THE  LAKYNX. 


Acute  Catarrhal  Laryngitis. — Chronic  Catarrhal  Laryngitis. — (Edema 

Glottidis. 


GEISTTLEMEIST  : — We  are  about  to  commence  the  study  of 
diseases  of  the  respiratory  organs,  and  most  naturally,  dis- 
eases of  the  larynx  will  first  engage  our  attention. 

Laryngeal  affections  may  be  primary  or  secondary : — pri- 
mary, when  the  larynx  is  the  part  first  affected,  and  the 
affeciion  is  local, — secondary,  when  the  laryngeal  disease 
occurs  as  a  complication,  and  depends  upon  some  morbid 
state  of  the  general  system. 

I  shall  consider  these  affections  under  the  following 
heads 

Fir?t. — Catarrhal  laryngitis,  which  may  be  acute  or 
chronic . 

Second. — (Edema  glottidis,  or  inflammation  of  the  submu- 
cous  tissue  of  the  larynx. 

Third. — Membranous  croup,  or  croupous  laryngitis, 
which  is  always  acute. 

Fourth. — Ulcerations,  which  may  be  catarrhal,  typhous> 
variolous,  tubercular,  or  syphilitic. 

Fifth. — Nervous  affections,  as  spasms,  paralysis,  etc. 

Sixth. — Pathological  new  formations,  as  polypi,  cancer, 
tubercle,  ossification  and  calcification  of  the  laryngeal  car- 
tilages. 

The  most  important  and  interesting  to  the  general  prac- 


2  DISEASES   OF  THE  LAEYNX. 

titioner  in  this  list  of  affections  are  inflammations,  and  to 
these  I  shall  now  direct  your  attention. 

ACUTE  CATARRHAL  LARYNGITIS. 

This  form  of  laryngitis  is  an  inflammation  of  the  mucous 
membrane  of  the  larynx,  which  gives  only  the  products  of 
catarrhal  inflammation.  It  may  occur  at  any  age,  and  be 
mild  or  severe  in  type  ;  the  severity  varies  in  proportion  to 
the  extent  that  the  submucous  areolar  tissue  of  the  larynx 
participates  in  the  morbid  processes. 

MORBID  ANATOMY. — The  anatomical  changes  which  take 
place  in  this  affection  are  characterized  by  redness,  swelling, 
and  softening  of  the  mucous  membrane  of  the  larynx ;  its 
surface  is  coated  with  mucus  which  contains  cells  predomi- 
nantly epithelial,  or  of  the  character  of  pus-cells.  When 
the  deeper  tissues  are  affected,  the  inflammatory  products 
accumulate  beneath  the  mucous  membrane,  as  well  as  in  its 
substance  and  upon  its  surface,  and  cause  tumefaction  of 
the  parts,  which  in  this  situation  is  attended  with  danger. 
On  the  other  hand,  when  the  inflammatory  process  is  super- 
ficial, and  all  the  products  are  upon  the  surface  of  the  mem- 
brane, there  is  little  danger. 

At  the  post-mortem  examination  there  is  often  less  red- 
ness and  swelling  of  the  laryngeal  membrane  than  was 
observed  during  life,  owing  to  the  richness  in  elastic  tissue 
of  this  mucous  membrane.  The  redness  and  swelling  are 
due  to  hypersemia  ;  probably  the  swelling  is  also  somewhat 
due  to  infiltration  and  increased  size  of  the  mucous  follicles. 

The  mucus  may  be  the  result  of  an  abnormal  secretion  of 
the  mucous  glands,  as  well  as  an  increased  degeneration  of 
the  epithelial  cells.  The  cells,  which  resemble  pus-cells, 
are  either  deviations  from  the  epithelium,  by  endogenous 
formations  (cast-off  epithelial  cells),  or  cells  of  the  mucous 
glands  ;  possibly,  some  are  the  white  blood-globules  which 
have  passed  through  the  walls  of  the  vessels. 

This  inflammation  usually  runs  a  rapid  course,  yet  in 
some  cases  it  becomes  chronic.  It  may  produce  erosions 
or  ulcers, — it  may  also  be  accompanied  by  ecchymoses  of 
the  membrane,  and  an  escape  of  blood  in  the  secretions  j 


ETIOLOGY.  3 

it  is  then  designated  hemorrhagic,  and  the  hemorrhage  is 
due  to  rupture  of  capillary  vessels.  Again,  in  some  cases  it 
is  limited  to  parts  of  the  larynx,  more  especially  to  the  epi- 
glottis ;  then  it  is  usually  associated  with  inflammation  of 
the  mouth,  fauces,  and  pharynx. 

The  danger  in  this  form  of  laryngitis  is  not  only  due  to 
the  submucous  inflammation,  but  also  to  the  spasm  of  the 
glottis,  which  the  infiltration  causes,  partly  by  reflex  action, 
partly  by  direct  irritation  of  the  adductor  muscles  of  the 
vocal  bands. 

ETIOLOGY. — Badly  nourished  cachectic  subjects,  rather 
than  the  strong  and  healthy,  are  predisposed  to  catarrhal 
laryngitis ;  those  in  the  open  air,  constantly  exposed  to 
changes  of  temperature,  are  less  liable  to  be  affected  with 
this  form  of  inflammation  than  those  who  rarely  are  sub- 
jected to  such  exposures. 

There  is  also  a  peculiar  vice  of  constitution  that  renders 
certain  persons  especially  liable  to  catarrhal  inflammation, 
and  consequently  predisposes  them  to  attacks  of  catarrhal 
laryngitis.  Among  the  exciting  causes  of  this  affection  may 
be  named  chilling  of  the  surface  by  exposure  to  wet  and 
cold,  particularly  that  of  the  neck  and  feet ;  mechanical  vio- 
lence to  the  larynx,  inhalation  of  irritating  vapors  and  acrid 
liquids  may  give  rise  to  the  most  intense  laryngeal  catarrh. 

Laryngitis  may  also  be  developed  secondarily  during  the 
course  of  the  exanthematous  fevers,  typhus  fever,  diph- 
theria and  syphilis, — not  unfrequently  it  is  the  result  of  the 
extension  of  inflammation  from  parts  adjacent  to  the  larynx, 
as  in  tonsillitis,  erysipelas,  etc.  Morbid  growths  and  ulcers 
of  the  larynx  are  accompanied  by  more  or  less  laryngeal 
catarrh.  The  catarrhal  laryngitis  which  is  always  present 
in  influenza  must  be  regarded  as  a  constitutional  or  infec- 
tious disorder.  Acute  bronchitis  is  usually  attended  by  a 
mild  form  of  laryngeal  catarrh. 

SYMPTOMS. — The  symptoms  that  attend  the  development 
of  catarrhal  laryngitis  vary  with  the  extent  and  severity  of 
the  inflammatory  process ;  its  approach  is  very  insidious, 
and  a  slight  laryngeal  catarrh  may  suddenly  become  very 
severe  in  character. 


4  ACUTE   CATARRHAL  LARYNGITIS. 

Usually  at  first  there  is  soreness  of  the  throat,  accompa- 
nied by  a  sense  of  constriction,  or  a  tickling  sensation  with 
a  tendency  to  cough  ;  the  larynx  is  tender  on  pressure, 
there  is  difficulty  in  swallowing,  which  becomes  more  and 
more  marked  as  the  disease  progresses  ;  to  this  is  soon  added 
difficulty  of  breathing. 

The  character  of  the  respiration  varies  with  the  seat  of  the 
inflammation.  If  it  is  confined  exclusively  to  the  upper  por- 
tion of  the  larynx,  as  it  often  is  at  the  onset  of  the  disease, 
the  difficulty  will  be  with  inspiration  only,  which  will  be 
prolonged  and  accompanied  with  stridor, — if  the  lining 
membrane  of  the  whole  larynx  is  involved,  and  the  calibre 
of  the  larynx  becomes  contracted  from  oedematous  infiltra- 
tion and  spasmodic  approximation  of  the  vocal  cords,  there 
will  be  difficulty  with  both  inspiration  and  expiration,  and 
both  will  be  protracted  and  wheezing ;  in  severe  cases  the 
patient  spends  all  his  energies  on  the  respiratory  acts,  and  he 
will  be  unable  to  lie  down.  There  is  a  harsh,  stridulous 
cough,  with  (at  first)  little  or  no  expectoration :  if  there  is 
any,  it  is  tenacious ;  later  it  may  become  thick,  purulent,  and 
abundant.  The  voice  is  hoarse  or  is  reduced  to  a  whisper. 
These  local  symptoms  are  accompanied  by  a  flushed  face,  a 
hot,  dry  skin,  the  temperature  often  rising  as  high  as  105°  P. 
The  pulse  is  frequent  and  hard  in  character.  In  severe  cases, 
as  the  disease  advances,  both  acts  of  respiration  become 
more  and  more  labored,  the  cough  more  and  more  metallic 
in  character, — the  patient's  distress  increases,  symptoms  of 
imperfect  aeration  of  the  blood  are  developed,  the  counte- 
nance becomes  pale  and  anxious,  or  livid.  During  the  exa- 
cerbations caused  by  spasm  of  the  laryngeal  muscles,  suffo- 
cation seems  imminent ;  in  the  intervals,  the  patient  be- 
comes drowsy,  the  vesicular  murmur  over  both  lungs  is 
feeble  or  is  no  longer  audible,  the  capillary  circulation  in 
the  extremities  is  imperfect,  the  lips  and  nails  become  blue, 
a  cold  perspiration  breaks  over  the  surface,  the  respiratory 
sounds  become  gurgling  and  gasping  in  character,  and  final- 
ly delirium  and  coma  close  the  scene. 

As  soon  as  the  characteristic  symptoms  of  acute  catarrhal 
laryngitis  are  manifest,  a  laryngoscopic  examination  will 


DIFFERENTIAL   DIAGNOSIS.  0 

show  the  mucous  membrane  of  the  larynx  to  be  of  a  bright 
red  color, — if  the  case  is  severe,  oadema  soon  appears,  the 
parts  being  red,  swollen,  and  semi-transparent.  The  tumefac- 
tion will  be  most  marked  on  the  ventricular  folds,  which  may 
entirely  conceal  from  view  the  vocal  bands  ;  this  redness  and 
tumefaction  may  extend  into  the  trachea,  or  it  may  be  con- 
fined to  the  mucous  membrane  of  the  larynx  and  free  bor- 
ders of  the  epiglottis. 

Death  may  occur  in  a  few  hours,  or  it  may  be  delayed 
five  or  six  days  ;  it  is  caused  by  a  complete  closure  of  the 
rima  glottis  from  tumefaction  of  the  mucous  and  submu- 
cous  tissues,  or  the  patient  struggles  on  with  obstructed 
respiration  and  dies  from  pulmonary  or  cerebral  congestion 
and  oedema. 

Death  may  take  place  very  suddenly,  from  the  combined 
effects  of  cedematous  swelling  and  spasm  of  the  glottis. 
When  the  disease  is  fatal,  its  course  is  usually  rapid  and 
severe, — when  recovery  takes  place,  it  is  mild  in  character 
and  extends  over  a  period  of  seven  or  eight  days. 

DIFFERENTIAL  DIAGNOSIS. — The  affections  which  may  be 
confounded  with  acute  catarrh  of  the  larynx  are  croupous 
laryngitis,  diphtheria,  oedema  of  the  larynx,  spasmodic  asth- 
ma, hysterical  laryngeal  spasm,  and  thoracic  aneurism. 

In  very  young  children  it  is  often  impossible  to  distin- 
guish between  catarrhal  laryngitis  and  croupous  laryngitis  ; 
but  when  the  laryngoscope  can  be  used,  the  presence  or  ab- 
sence of  false  membrane  decides  the  question. 

The  history  of  the  attack  and  the  accompanying  constitu- 
tional symptoms,  and  a  careful  laryngoscopic  examination, 
will  enable  you  readily  to  distinguish  between  the  laryngeal 
symptoms  of  acute  laryngitis  and  those  of  diphtheria,  oedema 
glottidis,  and  laryngeal  spasm ;  while  a  physical  examina- 
tion of  the  thorax  determines  the  existence  or  non-existence 
of  spasmodic  asthma  and  thoracic  aneurism. 

PROGNOSIS. — The  age  of  the  patient  is  the  most  important 
element  of  prognosis.  In  early  life,  this  disease  is  always 
attended  with  danger  ;  in  adults,  the  danger  depends  upon 
the  amount  of  oedema  present.  Its  tendency  in  all  severe 
cases  is  to  a  fatal  termination,  although  in  many  cases  death 


6  ACUTE   CATAKPJIAL   LARYNGITIS. 

may  be  prevented  or  at  least  delayed  by  the  performance  of 
tracheotomy  ;  yet  there  is  always  danger  that  the  inflamma- 
tion will  extend  down  the  trachea,  and  bronchitis  and  pneu- 
monia supervene. 

TREATMENT. — When  active  febrile  symptoms  are  present 
in  the  early  stage  of  acute  catarrhal  laryngitis,  occurring  as 
a  primary  disease  in  a  strong,  robust  adult,  venesection  to 
syncope  may  be  of  service  ;  but  if  the  symptoms  which  indi- 
cate imperfect  aeration  of  the  blood  are  present,  or  if  the 
laryngitis  is  a  secondary  affection,  venesection  is  not  only 
useless  but  does  positive  harm.  There  is  no  reliable  evi- 
dence that  local  depletion  by  leeches,  the  application  of 
blisters,  or  the  internal  administration  of  antimony  or  calo- 
mel have  any  power  to  arrest  the  progress  or  alleviate  any 
of  the  distressing  symptoms  of  this  disease. 

It  has  been  claimed  that  when  the  disease  involves  but  a 
small  portion  of  the  larynx,  the  direct  application  of  a  solu- 
tion of  nitrate  of  silver,  eighty  or  even  ninety  grains  to  the 
ounce,  to  the  inflamed  portion  by  means  of  a  sponge,  camel' s- 
hair  brush,  or  with  a  laryngeal  nebulizer,  speedily  relieves 
the  dyspnoea  and  ameliorates  the  general  symptoms.  Few, 
however,  have  the  requisite  skill  and  experience  in  topical 
medication  to  the  larynx  to  make  such  applications  effica- 
cious, or  at  least  to  accomplish  what  is  claimed  for  them. 
Most  practitioners  would  do  much  more  harm  than  good 
were  they  to  attempt  to  make  such  applications  in  acute 
laryngitis.  For  the  successful  management  of  this  disease  a 
warm,  moist,  and  uniform  temperature  is  essential ;  the  tem- 
perature of  the  apartment  should  never  be  allowed  to  fall 
below  76°  F.  When  the  submucous  areolar  tissue  is  either 
not  at  all  or  only  slightly  involved,  vapor  inhalations  un- 
questionably give  the  greatest  relief,  and  have  greater  power 
in  arresting  the  inflammatory  process  than  all  other  local 
means  which  the  general  practitioner  can  carry  out ;  they 
should  be  commenced  early  and  perseveringly  continued. 

The  internal  remedy  which  seems  to  have  the  power  of 
controlling  and  arresting  this  disease,  if  its  administration 
is  commenced  early,  is  the  sulphate  of  quinine  ;  it  must  be 
given  in  large  doses,  and  the  patient  brought  as  speedily  as 


MOEBID   ANATOMY.  7 

possible  into  a  state  of  cinchonism.  During  the  first  twenty- 
four  hours  I  would  advise  the  administration  of  twenty 
grains  to  a  child  three  years  of  age  suffering  with  a  severe 
form  of  laryngeal  catarrh. 

If  the  inflammatory  process  is  not  arrested  by  the  com- 
bined action  of  these  remedies,  oedema  is  almost  sure  to  fol- 
low, and  the  parts  should  be  freely  scarified  ;  in  the  adult  this 
may  be  readily  done  with  a  laryngeal  lancet  by  the  aid  of 
the  laryngoscope.  Should  this  treatment  fail  or  be  impossi- 
ble, and  should  the  dyspnoea  be  of  a  threatening  character, 
and  the  sign  of  imperfect  aeration  of  the  blood  be  well 
marked,  tracheotomy  must  not  be  delayed  ;  many  lives  have 
been  lost  by  too  long  delaying  this  operation. 

For  the  successful  management  of  acute  laryngitis,  rest  to 
the  larynx  is  all-important. 

CHRONIC  CATARRHAL  LARYNGITIS. 

Tins  disease  is  essentially  a  chronic  inflammation  of  the 
lining  membrane  of  the  larynx,  in  which  the  vessels  of  the 
areolar  tissue  very  slightly  participate. 

When  once  fully  established,  the  tendency  of  this  affec- 
tion is  to  remain  stationary. 

Like  the  acute,  it  may  be  general  or  partial. 

MOEBID  ANATOMY. — In  fully  developed  chronic  laryngeal 
catarrh,  the  mucous  surface  of  the  larynx  is  always  more  or 
less  coated  with  mucus  or  pus.  Its  tissue  is  dark-colored, 
sometimes  of  a  grayish  red  or  bluish  hue,  owing  to  previous 
ecchymoses, — it  is  either  softer  or  firmer  than  natural, — the 
mucous  glands  are  large  and  prominent, — the  submucous 
tissue  is  thickened,  and  the  bands  may  either  become  re- 
laxed or  stiffened,  and  hence  vibrate  less  than  in  health. 

As  a  result,  erosions,  fissures,  ulcerations,  hypertrophies, 
mucous  polypi,  or  small  papillary  excrescences  may  oc- 
cur ;  and  if  the  ulcerations,  as  they  may  in  depraved  states 
of  the  system,  should  penetrate  deeply,  they  may  occasion 
diseases  of  the  cartilages ;  sometimes  considerable  narrow- 
ing of  the  larynx  may  be  produced  by  the  submucous 
thickenings  and  chronic  cedema.  The  epiglottis  often  is 
eroded  when  elsewhere  no  ulceration  can  be  detected. 


8  CHRONIC   CATARRHAL   LARYNGITIS. 

When  the  trachea  is  involved,  that  portion  of  the  mucous 
membrane  covering  the  rings  is  reddened,  while  the  interme- 
diate portions  are  of  a  dark  gray  color. 

ETIOLOGY. — This  affection  may  occur  as  a  primary  dis- 
ease, or  as  a  sequela  of  acute  laryngitis  ;  not  unfrequently 
it  is  the  result  of  a  pharyngeal  inflammation  in  those  who 
use  alcohol  and  tobacco  in  excess,  and  in  those  who  con- 
stantly use  the  voice  in  public  speaking  and  singing.  It 
constitutes  the  chief  morbid  condition  in  what  is  termed 
"clergyman's  sore-throat."  The  constant  inhalation  of 
irritating  particles  may  be  a  cause  of  chronic  laryngitis ; 
but  it  most  frequently  occurs  as  an  accompaniment  of  other 
affections,  as  syphilis,  pulmonary  phthisis,  laryngeal  morbid 
growths,  etc. 

On  account  of  its  great  frequency  in  phthisical  and  sy- 
philitic subjects,  you  will  find  it  described  in  your  books 
under  the  head  of  laryngeal  phthisis,  and  syphilitic  laryn- 
gitis (it  is  one  of  the  later  manifestations  of  syphilis). 
These  are  only  varieties  of  chronic  laryngitis,  and  cannot  be 
regarded  as  distinct  forms  of  disease. 

That  variety  which  is  the  result  of  the  extension  of  a  fol- 
licular  faucitis  has  been  described  under  the  head  of 
chronic  glandular  laryngitis,  but  is  nothing  more  than  a 
laryngeal  catarrh  in  which  the  minute  racemose  glands  are 
principally  affected. 

The  sudden  development  of  the  larynx  in  males  which 
takes  place  at  puberty  is  often  attended  by  a  mild  form  of 
laryngeal  catarrh. 

In  every  variety  of  chronic  bronchitis,  especially  that  oc- 
curring in  old  age,  there  is  more  or  less  chronic  laryngeal 
catarrh, — in  many  instances  the  laryngeal  catarrh  is  second- 
ary to  the  bronchitis. 

SYMPTOMS. — The  symptoms  of  chronic  catarrhal  laryngitis 
are  altogether  local  in  character.  The  most  characteristic 
are  the  changes  which  occur  in  the  voice  ;  in  some  it  is 
hoarse  and  husky,  in  other  cases  the  patient  is  only  able  to 
speak  in  a  husky  whisper.  Accompanying  or  preceding 
the  vocal  changes  there  is  a  hoarse,  stridulous  cough,  with 
more  or  less  abundant  muco-purulent  or  purulent  expec- 


SYMPTOMS.  9 

toration ;  not  unfrequently  the  expectoration  is  streaked 
with  blood  and  of  a  fetid  odor. 

Both  respiratory  acts  are  more  or  less  impeded,  and  are 
often  accompanied  by  a  whistling  or  stridulous  sound,  and 
moist  rales  can  usually  be  heard  over  the  larynx. 

There  is  soreness  and  tenderness  of  the  laryngeal  carti- 
lages when  pressed  laterally  or  backward  against  the  spine. 

In  some  cases  the  act  of  swallowing  fluids  or  solids  is 
attended  with  no  inconvenience ;  in  other  cases  it  excites 
spasm  of  the  glottis,  and  thus  occasions  fits  of  distressing 
dyspnosa. 

If  constitutional  symptoms  exist,  they  are  due  to  sympa- 
thetic irritation,  and  are  in  no  way  characteristic  of  the 
disease. 

The  principal  danger  is  from  chronic  laryngeal  oedema, 
but  this  is  of  exceedingly  rare  occurrence. 

The  laryngoscopic  appearances  correspond  to  those 
changes  already  described  under  the  head  of  morbid 
anatomy  of  the  disease.  By  the  use  of  the  laryngoscope, 
general  or  partial  hypersemia  of  the  lining  membrane  of  the 
larynx  is  apparent ;  sometimes  the  larynx  has  the  appear- 
ance of  being  very  much  dilated,  at  other  times  it  is  appa- 
rently contracted.  The  mucous  surface  is  covered  over  with 
a  muco-purulent  secretion,  or  it  presents  a  dry  and  shining 
appearance  ;  again  the  enlarged  orifices  of  the  glands  may 
be  seen  as  pale  specks  on  the  congested  membrane,  or  as  red 
circles  studding  a  pale  membrane. 

In  addition  to  the  appearances  usually  presented  in 
chronic  laryngitis,  in  that  form  which  is  met  with  in  phthis- 
ical and  syphilitic  subjects,  there  is  found  more  or  less 
extensive  thickening,  ulceration,  and  papillary  excrescences 
are  sometimes  visible. 

In  the  chronic  laryngitis  of  phthisis,  a  chronic  oedema  of 
one  or  both  ary-epiglottic  folds  is  often  observed,  which  is 
almost  diagnostic  of  the  phthisical  origin  of  the  other 
changes  which  may  be  present. 

DIFFERENTIAL  DIAGNOSIS.  —  The  diagnosis  of  chronic 
laryngitis  is  readily  made  ;  the  changes  in  the  voice  at  once 
direct  the  attention  to  the  larynx,  and  with  the  laryngo- 


10  CHEONIC    CATAREHAL  LARYNGITIS. 

scope  you  may  determine  the  nature,  extent,  and  exact  seat 
of  the  disease. 

From  the  general  and  local  symptoms,  chronic  laryngitis 
may  be  confounded  with  laryngeal  growths  and  nervous 
affections  of  the  larynx,  but  a  careful  laryngoscopical  exami- 
nation will  correct  any  error. 

Its  connection  with  pulmonary  phthisis  may  be  determined 
by  a  careful  physical  examination  of  the  lungs.  Its  syph- 
ilitic origin  may  be  determined  by  the  history  of  the  patient. 
If  both  phthisis  and  syphilis  be  excluded,  the  disease  must 
be  regarded  of  primary  origin. 

PROGNOSIS. — The  prognosis  in  this  affection  depends  on 
its  pathological  associations.  In  connection  with  pulmo- 
nary phthisis,  recovery  is  of  rare  occurrence ;  when  it  depends 
upon  syphilis,  the  prospect  of  recovery  is  much  better,  al- 
though the  voice  is  likely  to  remain  permanently  affected. 

All  other  forms  of  chronic  ]aryngitis,  unless  some  compli- 
cation occur,  may  be  recovered  from ;  at  least,  they  rarely  if 
ever  lead  to  a  fatal  termination.  It,  however,  is  always 
difficult,  and  sometimes  impossible,  to  cure  chronic  laryngitis 
in  old  people. 

TREATMENT. — The  most  important  agents  in  the  treatment 
of  chronic  laryngitis  are  local  remedies  applied  within  the 
larynx  to  the  parts  affected.  These  topical  applications 
may  be  made  at  the  time  of  a  laryngoscopical  examination, 
either  by  means  of  a  sponge  or  camel' s-hair  brush  carried 
within  the  larynx — by  the  inhalation  of  vapor  impregnated 
with  some  volatile  substance — or  in  the  form  of  nebulized 
liquids. 

The  most  certain  and  satisfactory  method  is  by  means  of 
i-  sponge  or  camel' s-hair  brush.  The  topical  remedy  most 
frequently  employed  is  the  nitrate  of  silver,  sixty  grains  to 
an  ounce  of  water.  Many,  however,  prefer  a  solution  of  the 
cluoride  of  zinc,  thirty  grains  to  an  ounce  of  glycerine  ;  if 
the  applications  are  made  directly  to  the  diseased  tissues, 
and  sufficiently  often,  it  matters  very  little  what  astringent 
solution  is  used.  When  the  laryngeal  secretion  is  excessive, 
the  local  application  of  turpentine  sometimes  does  good. 

For  steam  inhalations,  a  few  drops  of  oil  of  creosote,  oil  of 


MOKBID   ANATOMY.  11 

pine  or  oil  of  juniper,  added  to  half  a  pint  of  water  at  a  tem- 
perature of  150°  F.,  may  be  employed.  * 

For  spray  inhalations — a  solution  of  alum,  perchloride  of 
iron,  tannin,  or  the  sulphate  of  zinc,  from  one  to  twenty 
grains  to  the  ounce  of  water  may  be  used. 

Neither  the  steam  nor  spray  inhalations  should  be  con- 
tinued more  than  five  minutes  at  a  time  ;  they  may  be 
repeated  three  or  four  times  during  the  twenty-four  hours. 
A  solution  of  carbolic  acid  (two  grains  to  the  ounce  of 
water),  either  as  a  spray  or  as  a  steam  inhalation,  may  be 
used  with  benefit  in  cases  where  the  laryngeal  secretion  has 
a  fetid  odor. 

In  addition  to  the  local  treatment  of  the  larynx,  the 
patient  must  be  removed  from  all  sources  of  laryngeal  irri- 
tation. The  vocal  organs  must  have  absolute  rest — if  possi- 
ble the  patient  must  change  climate,  removing  to  such  as  he 
finds  best  suited  to  his  individual  case, — as  a  rule,  a  warm, 
dry  atmosphere  best  agrees  with  this  class  of  patients. 

The  constitutional  treatment  of  each  patient  will  be  gov- 
erned by  his  general  condition,  and  the  pathological  rela- 
tions of  the  laryngitis.  If  it  is  of  phthisical  origin,  the 
general  treatment  of  phthisis  is  indicated  ;  if  it  is  traceable 
to  syphilis,  the  anti-syphilitic  remedies  must  be  resorted  to  ; 
occurring  as  it  does  among  the  later  manifestations  of  syph- 
ilis, the  iodide  of  potassium  will  usually  be  found  of  ser- 
vice. 

The  general  hygiene  of  the  patient  should  be  carefully  at- 
tended to  in  the  mild  as  well  as  in  severe  forms  of  chronic 
laryngitis. 

(EDEMA.  GLOTTIDIS. 

(Edema  glottidis  is  a  term  which  has  been  used  to  indi- 
cate the  occurrence  of  dropsical  effusion  or  inflammatory  ex- 
udations in  the  areolar  tissue  beneath  the  laryngeal  mem- 
brane, above  the  vocal  bands.  Strictly  speaking,  it  is  not 
OBdema  of  the  glottis  but  of  the  upper  portion  of  the  larynx. 
Its  gravity  and  the  necessity  for  its  prompt  relief  make  it 
important  that  you  should  recognize  its  existence,  and  more 
than  this,  that  you  should  appreciate  the  pathological 


12  (EDEMA   GLOTTIDIS. 

conditions  which  lead  to  its  recurrence  and  attend  its  de- 
velopment. 

MOKBID  ANATOMY. — The  effusion,  which  is  almost  always 
serous,  takes  place  in  the  loose  cellular  tissue  beneath  the 
mucous  membrane  of  the  upper  part  of  the  larynx,  princi- 
pally in  the  ary-epiglottic  folds,  and  at  the  base  of  the 
epiglottis  ;  as  a  consequence,  these  parts  become  prominent 
and  the  epiglottis  is  swollen.  On  either  side  there  may  be  a 
tumor  an  inch  or  more  in  diameter,  projecting  into  the  cav- 
ity of  the  larynx  and  pharynx, — in  some  cases  these  tumors 
touch  each  other,  completely  occluding  the  laryngeal 
cavity.  The  mucous  membrane  may  be  either  red  or  pale. 
On  pricking  the  tumors,  a  clear,  or  a  turbid,  or  even  a  pur- 
ulent fluid  escapes,  after  which  the  parts  previously  dis- 
tended collapse,  and  the  mucous  membrane  is  left  wrinkled 
and  folded.  The  effusion  may  occur  wholly  or  principally 
on  one  side. 

Not  unfrequently  after  death,  owing  to  the  disappear- 
ance of  the  effusion,  the  wrinkled  condition  of  the  mucous 
membrane  is  all  that  is  found,  or  at  least  there  is  much  less 
effusion  than  might  have  been  expected  from  the  appear- 
ance of  the  parts  during  life. 

ETIOLOGY. — (Edema  of  the  glottis  rarely  if  ever  occurs  as 
an  idiopathic  affection,  but  is  secondary  to,  or  a  complica- 
tion of,  some  local  laryngeal  disease  or  constitutional  disor- 
der. Any  inflammatory  affection  of  the  larynx  or  of  the 
tissues  adjacent  may  give  rise  to  it — such  as  acute  laryngi- 
tis (especially  that  due  to  local  irritation),  erysipelas  of 
the  neck,  deep-seated  cervical  abscesses,  and  acute  tonsillitis. 
It  occasionally  occurs  as  a  complication  of  the  laryngeal 
ulceration  of  typhus  and  typhoid  fever,  small-pox,  and 
scarlatina.  Sometimes  it  is  the  immediate  cause  of  death  in 
the  general  dropsy  of  Bright' s  disease,  and  in  the  venous 
obstruction  which  attends  some  forms  of  cardiac  disease 
and  thoracic  aneurism. 

SYMPTOMS. — The  prominent  symptom  of  this  affection  is 
dyspnoea,  and  the  difficulty  in  breathing  is  mainly  confined 
to  inspiration.  No  difficulty  in  swallowing  is  experienced, 
nor  is  there  any  tenderness  on  pressure  over  the  larynx 


DIFFERENTIAL  DIAGNOSIS.  13 

Fever  and  the  other  constitutional  symptoms  which  attend 
acute  laryngitis  are  absent.  It  is  accompanied  by  parox- 
ysms of  strangulation, — suffocative  breathing  is  usually  the 
first  indication  of  its  occurrence ;  there  is  also  an  uneasy 
sensation  in  the  region  of  the  larynx,  and  a  constant  incli- 
nation on  the  part  of  the  patient  to  rid  the  upper  part  of 
the  throat  of  some  supposed  secretion. 

If  the  index  finger  be  carried  below  the  epiglottis,  oedem- 
atous  tumors  may  be  distinctly  felt.  Hoarseness  or  huski- 
ness  of  the  voice  may  not  be  present  unless  laryngitis  co- 
exist. 

The  laryngoscope  reveals  two  tense,  smooth,  rounded  swel- 
lings immediately  behind  the  epiglottis  ;  these  swellings  after 
meeting  in  the  centre,  with  a  sluice  between  them,  appear 
oval.  The  oedema  is  usually  much  marked  at  the  ventricu- 
lar folds,  which  explains  the  nature  of  the  urgent  dyspnoea. 

Whenever,  during  the  progress  of  any  of  the  diseases  in 
which  oedema  glottidis  is  liable  to  occur,  you  notice  the 
slightest  difficulty  in  laryngeal  respiration,  the  difficulty 
being  limited  to  inspiration,  you  should  be  on  your  guard 
as  to  the  possible  occurrence  of  this  accident. 

DIFFERENTIAL  DIAGNOSIS.  —  The  circumstances  under 
which  oedema  glottidis  is  developed,  the  suddenness  of  its 
occurrence,  the  peculiar  character  of  the  respiration  indicat- 
ing obstruction  at  the  upper  portion  of  the  larynx,  and  the 
absence  of  febrile  excitement,  afford  almost  positive  evidence 
of  its  existence.  When  to  these  are  added  the  feel  of  the 
oedematous  tumors  and  the  laryngoscopic  view  of  their  size 
and  situation,  the  differential  diagnosis  between  it  and  other 
laryngeal  affections  is  easily  made. 

PROGNOSIS. — The  tendency  of  this  affection  is  to  speedily 
destroy  life,  but  in  most  instances  it  may  be  saved  by  prompt 
and  efficient  surgical  interference. 

TREATMENT. — There  is  no  time  to  be  lost  in  fruitless  medi 
cation.  In  extreme  cases  the  only  means  which  afford  you 
any  ground  for  hope  are  laryngotomy  or  tracheotomy,  either 
of  which  to  prove  efficacious  must  be  performed  early. 

It  is  recommended  by  some,  to  scarify  the  edges  of  the 
cedematous  epiglottis,  or  ventricular  bands  and  ary-epiglot- 


14  (EDEMA   GLOTTIDI3. 

tic  folds,  so  as  to  give  free  exit  to  the  effused  fluid,  before 
resorting  to  these  operations.  This  scarification  can  rarely 
be  accomplished  except  by  an  experienced  hand,  and  in 
extreme  cases  the  delay  and  danger  which  attend  such  an 
attempt  are  hardly  justifiable. 


LECTURE  II. 


DISEASES  OF  THE  LARYNX. 


Acute  Croupous  Laryngitis  (Membranous  Croup). — Ulcers  of  the  Larynx. 

CROUPOTJS  inflammation  of  the  larynx  differs  from  ca- 
tarrlial,  in  the  nature  of  the  inflammatory  products  ;  in  the 
former  they  consist  mainly  of  fibrine,  in  the  latter,  of  mu- 
cus. In  croupous  laryngitis  the  inflammatory  process  may 
be  limited  to  the  larynx,  or  it  may  extend  into  the  trachea 
and  bronchi, — trachitis  so  frequently  accompanies  it,  that 
the  disease  has  received  the  name  of  cjmanche  trachealis, 
but  in  all  instances  the  tracheal  inflammation  is  secondary 
to  the  laryngeal.  I  shall  consider  croupous  laryngitis  as  a 
local  inflammation,  having  an  entirely  distinct  history  from 
the  infectious  disease  known  as  diphtheria. 

MORBID  Ax  ATOMY. — In  this  form  of  laryngitis  there  exists 
over  a  varying  extent  of  the  mucous  membrane  a  whitish  or 
yellowish-white  fibrinous  layer,  often  spotted  here  and  there 
with  dots  or  lines.  This  membranous  exudation  may  be 
limited  to  a  few  patches,  or  form  a  cylinder  which  may  ex- 
tend itself  into  the  trachea  and  bronchi.  At  one  time  it  is 
firm  in  its  consistence,  and  tenaciously  adheres  to  the  sub- 
jacent membrane,  while  at  another  time  it  is  soft  and  easily 
separated  from  the  subjacent  membrane.  Its  thickness 
varies  ;  sometimes  it  is  scarcely  perceptible,  yet  it  may  have 
even  greater  thickness  than  a  line.  Its  surface  is  smooth,  it 
adheres  firmly  to  the  vocal  cords  and  the  upper  part  of  the 
epiglottis,  which  is  the  part  of  the  laryngeal  membrane  that 


16  ACUTE   CROUPOUS   LARYNGITIS. 

possesses  a  pavement  epithelium.  The  membrane  having 
been  formed,  it  may  be  cast  off  as  such  in  the  form  of  a 
cylinder,  bands,  or  shreds.  Its  separation  is  produced  by 
the  secretion  of  the  follicles  which  have  been  dammed  up, 
as  well  as  by  a  serous  exudation  from  the  previously  in- 
flamed membrane.  It  may  break  up  into  threads  and  be 
expectorated  as  such,  or  it  may  undergo  a  granular,  fatty, 
or  more  rarely  a  mucous  degeneration,  and  so  become  a 
fluid  resembling  mucus  ;  hence,  in  the  latter  case,  no  mem- 
branous exudation  can  be  observed. 

In  the  earlier  stages  the  mucous  membrane  of  the  larynx 
presents  the  same  appearance  as  in  catarrhal  inflammation. 

When  the  false  membrane  has  formed,  it  takes  the  place 
of  the  epithelium,  and  is  situated  on  the  homogeneous  boun- 
dary layer  of  the  mucous  membrane  which  exists  in  the 
greater  part  of  the  larynx  ;  this  tissue  is  pale,  except  when 
it  is  spotted  with  ecchymoses,  which  correspond  to  similar 
ones  in  the  membranous  exudation.  The  laryngeal  mem- 
brane is  somewhat  swollen  and  moister  than  natural. 

Generally  the  submucous  tissue  is  only  slightly  affected 
by  it,  and  rarely  is  it  the  seat  of  effusion  or  cell  formation. 

A  microscopic  examination  of  this  membranous  exudation 
shows  it  to  consist  of  a  homogeneous  shining  net-work,  in  the 
meshes  of  which  are  enclosed  pus  cells,  rarely  epithelium  ; 
it  may  be  made  up  of  alternate  layers  of  fibrine  and  cells. 
The  homogeneous  net-work  has  the  reaction  of  coagulated 
fibrine.  It  is  exuded  from  the  vessels  as  a  fluid,  and  coagu- 
lates upon  its  arrival  at  the  surface,  entangling  the  cells. 
It  is  a  question  whether  these  cells  are  changed  epithelial 
cells  or  white  globules.  The  mucous  membrane  contains  a 
varying  amount  of  these  cells,  as  do  all  inflamed  tissues. 
As  the  membranous  exudation  is  cast  off,  the  epithelium  on 
its  surface  is  quickly  repaired,  and  the  laryngeal  membrane 
returns  to  its  normal  condition.  After  the  membrane  is 
thrown  off,  it  may  be  reproduced  two  or  three  times.  The 
submucous  tissue  is  more  liable  to  be  affected  in  adults  than 
in  children. 

Yery  frequently  membranous  pharyngitis  precedes  and  i3 
associated  with  croupous  laryngitis,  and  the  croupous  in- 


ETIOLOGY.  17 

tiammation  (as  I  have  already  stated)  may  extend  to  the 
trachea  and  bronchi,  or  the  latter  may  only  be  in  a  state  of 
catarrhal  inflammation.  Pulmonary  congestion,  oedema, 
atelectasis,  emphysema,  and  lobnlar  pneumonia  not  unfre- 
quently  occur  as  complications  in  the  course  of  this  disease. 

ETIOLOGY. — Age  has  the  greatest  predisposing  influence 
to  this  disease.  It  is  of  rare  occurrence  among  adults  or 
very  young  infants  ;  the  time  of  greatest  liability  to  this  dis- 
ease is  the  interval  between  the  period  of  dentition  and  pu- 
berty. There  is  no  evidence  that  its  development  is  due  to 
any  specific  atmospheric  poison.  Exposure  to  cold  and 
moisture,  with  sudden  alterations  of  temperature,  are  among 
its  most  frequent  exciting  causes.  It  occurs  more  frequently 
during  the  winter  and  spring  months. 

Delicate,  weakly,  and  ill-nourished  children,  rather  than 
the  strong  and  healthy,  are  liable  to  this  disease.  It  not  un- 
frequently  follows  the  sudden  disappearance  of  eczematous 
eruptions  on  the  head  and  face ;  occasionally  it  follows 
measles,  scarlatina,  and  variola,  and  sometimes  complicates 
diphtheria. 

SYMPTOMS. — Acute  croupous  laryngitis  usually  begins 
with  the  ordinary  symptoms  of  a  simple  cold ;  at  its  com- 
mencement there  is  nothing  to  distinguish  it  from  an  ordi- 
nary catarrh.  If  the  throat  is  examined,  the  whole  visible 
mucous  membrane  will  be  found  red  and  tumefied.  Usually, 
the  first  symptom  that  attracts  attention  is  a  slight  hoarse- 
ness ;  a  little  later  the  respiration  becomes  difficult,  the  ex- 
piration noisy,  and  is  accompanied  by  a  high-pitched  strid- 
ulous  cough.  The  inspiration  that  immediately  follows  the 
cough  is  accompanied  by  a  loud  crowing  noise.  Although 
there  is  no  pain  nor  tenderness  in  handling  the  larynx  or 
trachea,  there  is  some  difficulty  in  swallowing,  and  the 
child  frequently  puts  his  hand  to  his  throat  as  if  to  remove 
some  obstruction.  With  the  first  croupy  paroxysm,  how- 
ever slight  in  degree,  the  pulse  is  accelerated,  and  is  full 
and  hard  in  character  ;  there  is  increased  heat  and  redness 
of  the  surface,  especially  of  the  face,  as  also  an  injection  of 
the  conjunctival  vessels  ;  the  axillary  temperature  may  range 
from  102°  F.  to  105°  F.  These  febrile  symptoms  somewhat 


18  ACUTE   CROUPOUS   LARYXGITIS. 

subside  as  the  paroxysm  passes  off,  to  return,  however,  with 
greater  intensity  on  the  return  of  the  next  paroxysm.  At 
the  commencement  of  the  attack  the  paroxysms  of  dysp- 
noea are  more  frequent  and  severe  at  night  than  during  the 
day.  As  the  disease  advances  the  voice  is  entirely  lost ;  the 
patient  speaks  and  cries  in  a  whisper ;  the  cough  is  sup- 
pressed and  becomes  more  and  more  stridulous  in  character, 
without  expectoration  ;  the  head  is  thrown  back ;  the  respira- 
tion grows  more  and  more  difficult,  and  with  each  inspira- 
tion there  is  contraction  of  the  lower  part  of  the  chest  and 
sinking  in  of  the  soft  parts  above  the  clavicles.  The  vesicu- 
lar murmur  over  both  lungs  is  feeble  or  inaudible ;  with 
every  inspiration  the  epigastrium,  instead  of  projecting,  is 
strongly  depressed,  and  the  outward  movement  of  the 
lower  ribs  is  arrested.  Every  muscle  that  can  aid  in  ex- 
panding the  chest  is  brought  into  violent  action.  During 
these  laborious  efforts  at  inspiration  the  nostrils  are  dilated. 
As  the  laryngeal  obstruction  increases,  the  paroxysms  of 
dyspnoaa  become  more  urgent  without  remission  ;  there  is 
a  restless  tossing  of  the  limbs,  and  the  greatest  terror  is 
depicted  on  the  face — at  one  time  it  is  pale,  at  another  livid ; 
the  pulse  becomes  rapid  and  feeble,  the  temperature  falls 
sometimes  below  the  normal  standard,  and  the  extremities 
become  cold. 

Gradually,  as  the  blood  becomes  imperfectly  aerated,  the 
patient  becomes  drowsy,  at  times  rousing  up  and  gasping 
for  air,  and  springing  from  one  place  to  another  to  find 
relief  ;  the  lips  and  nails  become  blue,  the  respiration  grows 
shorter  and  shorter,  until  at  last,  after  a  violent  paroxysm 
of  dyspnoaa,  he  becomes  unconscious  and  quietly  ceases  to 
breathe.  The  disease  always  attains  its  height  by  the  end 
of  the  third  day  ;  death  may  occur  within  forty-eight  hours 
after  its  commencement ;  its  whole  duration  rarely  exceeds 
five  days. 

In  accordance  with  its  symptomatology,  croupous  laryn- 
gitis may  be  divided  into  three  stages,  a  precursory  or  ca- 
tarrhal  stage,  a  stage  of  development,  and  a  suffocative  or 
stage  of  collapse.  The  most  important  fact  connected  with 
its  clinical  history  is,  that  in  a  large  proportion  of  cases. 


SYMPTOMS.  19 

before  the  urgent  symptoms  come  on,  the  membranous  ex- 
udation can  be  seen  on  the  tonsils.  In  nine  cases  out  of  ten 
the  membrane  is  first  formed  on  the  tonsils  or  in  their 
immediate  vicinity  ;  when  seen,  the  diagnosis  is  established 
before  the  urgent  symptoms  are  developed. 

As  the  membrane  extends  into  the  larynx  there  is  loss  of 
voice,  a  stridulous  cough,  difficult  breathing,  and  the  face 
is  alternately  flushed  and  pale. 

For  a  day  or  two,  while  the  membrane  is  extending  and 
becoming  thicker  and  thicker,  the  patient  remains  in  about 
the  same  condition,  gradually  growing  weaker,  the  capil- 
lary circulation  on  the  surface  becoming  more  and  more 
imperfect,  the  respiration  more  and  more  labored,  the  par- 
oxysms of  dyspnoea  more  and  more  frequent  and  severe, 
until  there  is  little  hope  of  recovery.  When,  sometimes,  all 
the  urgent  symptoms  are  suddenly  relieved,  the  patient 
coughs  and  a  stringy  matter  is  expectorated, — he  struggles 
for  a  moment  in  a  violent  paroxysm  of  dyspnoea,  and  a  per- 
fect membranous  cast  of  the  larynx,  and  perhaps  of  "the 
trachea  and  larger  bronchi,  is  expectorated.  Now  he  passes 
into  a  quiet  sleep,  and  recovery  seems  certain,  but  still  there 
is  great  danger — first,  from  the  formation  of  a  new  mem- 
brane in  the  larynx  and  trachea,  should  there  be  a  continu- 
ance of  the  inflammatory  process ;  second,  from  the  exten- 
sion of  the  inflammation  into  the  minute  bronchial  tubes, 
giving  rise  to  capillary  bronchitis  and  pneumonia  ;  third, 
from  the  exhaustion  that  has  occurred  before  the  membrane 
was  thrown  off. 

Laryngoscopy  is  scarcely  ever  practicable  in  the  class  of 
patients  in  which  this  disease  occurs.  The  membranous 
exudation  is  readily  seen,  and  its  extent  accurately  deter- 
mined whenever  a  laryngoscopic  examination  can  be  made. 

DIFFERENTIAL  DIAGNOSIS. — The  two  affections  of  the 
larynx  which  are  most  liable  to  be  confounded  with  the  one 
under  consideration  are,  simple  catarrh  of  the  larynx,  called 
spasmodic  or  pseudo-croup,  occurring  in  nervous  subjects, 
and  purely  spasmodic  affections  of  the  larynx.  In  each  of 
these  the  laryngeal  spasm  gives  rise  to  the  croupy  symp 
toms. 


20  ACUTE   CKOUPOUS   LARYNGITIS. 

In  spasmodic  croup  or  simple  catarrh  of  the  larynx,  the 
croupous  phenomena  come  on  suddenly, — the  attack  usu- 
ally occurs  at  night,  it  is  not  preceded  or  accompanied  by 
active  febrile  symptoms, — there  is  no  complete  loss  of  voice, 
and  there  is  absence  of  membranous  exudation  on  the  ton- 
sils and  epiglottis.  All  of  these  conditions  are  important 
diagnostic  features  of  croupous  laryngitis.  Besides,  within 
twenty-four  hours  after  the  commencement  of  an  attack  of 
catarrhal  croup,  auscultation  of  the  chest  furnishes  signs 
of  incipient  bronchial  catarrh. 

Spasm  of  the  glottis,  which  may  give  rise  to  croupy  symp- 
toms, is  excited  in  infancy  by  a  variety  of  causes.  Among 
these  are  dental  irritation,  gastric  irritation,  enlargement  of 
the  thy m us  gland,  giving  rise  to  what  is  called  thymic  asthma, 
and  undue  excitability  of  the  nervous  system,  the  result  of 
hereditary  predisposition.  These  laryngeal  spasms  may  be 
recognized  by  the  suddenness  and  violence  of  the  attack, 
by  the  absence  of  the  catarrhal  and  febrile  symptoms,  by 
the'  absence  of  alteration  in  the  voice,  and  by  the  speedy 
and  complete  relief  which  immediately  follows  the  spasm. 

Diphtheria  involving  the  larynx,  sometimes  mistaken  for 
croup,  may  be  distinguished  from  it  by  the  following  char- 
acteristics :  first,  diphtheria  is  either  epidemic,  or  there  is  a 
history  of  contagion  ;  second,  the  development  of  the  throat 
symptoms  is  generally  preceded  for  some  days  by  constitu- 
tional disturbances  ;  third,  the  glands  at  the  angle  of  the 
jaws  are  always  enlarged,  and  usually  the  laryngeal  symp- 
toms are  not  urgent ;  fourth,  the  pharynx  presents  the 
characteristic  diphtheritic  appearance  before  any  laryngeal 
symptoms  are  present. 

PROGNOSIS.— There  is  no  data  from  which  to  estimate  the 
ratio  of  mortality  in  this  disease  ;  unquestionably  it  is  one 
of  the  most  fatal  diseases  of  childhood.  When  the  diagno- 
sis is  based  upon  the  presence  of  the  membranous  exuda- 
tion on  the  tonsils  and  epiglottis,  recovery  seldom  occurs. 
The  signs  of  a  favorable  termination  are,  diminution  in  the 
frequency  and  severity  of  the  parox3rsms  of  dyspnoea,  with 
less  distress  in  breathing  during  the  intervals,  a  gradual  re- 
turn of  the  voice,  and  a  moist  sound  with  the  cough. 


TREATMENT.  21 

If,  on  the  other  hand,  the  paroxysms  of  dyspnoea  become 
more  frequent  and  violent,  the  restlessness  and  dyspnoea 
increase  during'  the  intervals,  and  the  cough  is  less  power- 
ful and  more  stridulous,  the  blueness  of  the  lips  and  nose 
more  marked,  and  the  patient  becomes  more  and  more 
drowsy, — recovery  is  scarcely  possible.  The  younger  the 
patient,  the  greater  the  danger.  In  fatal  cases,  the  duration 
of  the  disease  is  from  three  to  seven  days.  If  recovery  takes 
place,  it  is  slow,  weeks  often  elapsing  before  the  voice  is 
returned,  during  all  of  which  time  the  patient  is  subject  to 
violent  paroxysms  of  dyspnoea.  It  has  been  my  experience 
to  see  very  few  recover  when  my  diagnosis  was  beyond 
question. 

TKEATMEISTT. — I  do  not  purpose  to  discuss  the  merits  of 
the  various  plans  of  treatment  for  the  management  of  mem- 
branous croup  that  have  been  proposed  by  writers  on  that 
subject,  for  under  every  plan  the  disease  has  proved  fatal 
in  the  vast  majority  of  cases. 

Simple  catarrh  of  the  larynx  is  so  liable  to  be  mistaken 
for  croupous  laryngitis  that  it  is  difficult  to  estimate  the 
real  value  of  the  different  remedial  agents  which  it  has  been 
claimed  have  a  controlling  power  over  membranous  croup. 
The  statement  made  by  any  observer,  that  a  certain  plan 
followed,  or  agent  employed,  was  successful  in  the  majority 
of  cases  of  croup,  leads  one  who  has  relied  upon  the  visi- 
ble presence  of  the  membranous  exudation  for  his  diagnosis 
to  question  the  correctness  of  such  a  statement,  believing 
there  has  been  an  error  in  diagnosis. 

You  should  remember,  that  from  the  very  onset  of  the 
disease  you  have  to  do  with  a  peculiar  form  of  inflamma- 
tory action,  the  characteristic  of  which  is  a  membranous 
exudation,  and  that  with  our  present  therapeutical  knowl- 
edge we  know  of  no  agent  that  can  prevent  this  exudation. 
It  has  been  claimed  that  mercury  has  such  power  by  dimin- 
ishing the  plasticity  of  the  blood, — but,  with  the  written 
history  of  membranous  croup  before  us,  we  find  no  evidence 
that  calomel,  blood-letting,  or  antimony  have  any  power 
either  to  arrest  the  progress  of  the  inflammatory  action  or 
to  prevent  the  membranous  exudation. 


22  ACUTE  CROUPOUS   LARYNGITIS. 

In  the  treatment  of  this  affection  it  is  of  the  first  importance 
that  the  patient  should  be  placed  in  a  large,  well-ventilated 
apartment,  the  temperature  of  which  should  be  kept  uni- 
formly at  75°  F.  to  80°  F.,  and  the  air  rendered  moist  by  steam. 
In  the  case  of  children,  a  tent  may  be  made  over  the  bed  by 
means  of  blankets,  into  which  is  made  to  pass  a  constant 
current  of  steam  from  a  kettle  containing  boiling  molasses 
and  water  ;  as  soon  as  the  evidences  of  imperfect  oxygena- 
tion  are  apparent,  a  continuous  stream  of  oxygen  gas 
should  be  carried  into  the  tent,  or  arrangements  should  be 
made  so  that  it  will  be  constantly  inhaled  by  the  patient ; 
sometimes,  in  addition  to  these  means,  lime  vapor,  produced 
by  slacking  large  quantities  of  quicklime  in  the  room  will 
be  found  of  service.  During  the  whole  course  of  treatment 
sponges  dipped  in  boiling  water,  and  then  squeezed  as  dry  as 
possible,  should  be  kept  over  the  front  of  the  neck. 

Whenever  there  are  indications  that  loosened  portions  of 
membrane  act  as  a  producing  cause  of  the  dyspnoea,  an 
emetic  may  be  administered, — the  sulphate  of  zinc  acts  most 
promptly  and  efficaciously.  The  frequent  administration  of 
emetics  is  to  be  avoided,  on  account  of  their  depressing  influ- 
ence on  the  patient.  Topical  applications  are  not  to  be  re- 
sorted to  in  the  treatment  of  this  form  of  laryngitis,  as  they 
intensify  rather  than  relieve  the  laryngeal  spasm,  which 
plays  so  important  a  part  in  producing  the  paroxysms  of 
dyspnoea,  and  there  is  no  evidence  that  they  have  any  con- 
trol over  the  inflammatory  process. 

It  is  all-important  that  this  class  of  patients,  from  the  very 
onset  of  the  disease,  should  receive  a  most  nutritious  diet, 
and  as  failure  of  the  vital  powers  becomes  apparent,  stimu- 
lants may  be  freely  administered. 

As  regards  internal  medication,  I  have  little  confidence  in 
any  of  the  so-called  specific  remedial  agents  for  the  treat- 
ment of  this  aifection.  At  the  commencement  of  the  laryn- 
geal inflammation,  before  the  commencement  of  the  mem- 
branous exudation,  thirty  grains  of  the  sulphate  of  quinine, 
in  five-grain  doses,  may  be  beneficially  administered  to  a 
child  three  years  of  age,  with  the  intent  of  arresting  the 
inflammatory  process,  and  I  believe  I  have  the  evidence  that 


MORBID   ANATOMY.  23 

quinine  thus  administered  has  prevented  catarrhal  laryn- 
gitis from  becoming  croupous.  After  the  formation  of  the 
membranous  exudation,  the  vapor  inhalation  and  the  oxy- 
gen gas  are  the  only  means  which  furnish  any  hope  that  the 
patient  can  be  safely  carried  through  the  disease. 

Lastly,  the  propriety  of  tracheotomy  in  membranous 
croup  presents  itself.  The  opinion  of  the  profession  is 
divided  upon  this  subject.  The  statistics  of  this  operation 
in  this  disease  are  not  to  be  relied  upon.  The  only  question 
to  settle  is,  Has  one  life  been  saved  by  it  ?  If  this  can  be  an- 
swered affirmatively,  the  operation  is  justifiable.  It  never 
should  be  resorted  to  with  a  promise  even  of  relief  ;  if  there 
are  evidences  that  the  membranous  formation  has  reached 
the  bronchi,  and  even  when  the  membrane  has  formed  ill 
the  trachea,  temporary  relief  from  the  dyspnoea  is  all  that 
can  be  promised. 

The  operation,  to  be  successful,  must  be  performed  early  in 
the  progress  of  the  disease,  and  not  delayed,  as  it  usually  is, 
until  the  patient  is  beyond  hope  of  recovery.  Its  success 
also  undoubtedly  depends  much  upon  the  manner  of  its 
performance  and  upon  the  subsequent  management  of  the 
case. 

ULCERS   OF  THE  LARYNX. 

The  laryngeal  aifections  included  in  our  list  of  laryngeal 
diseases  that  still  remain  to  be  considered,  come  more  di- 
rectly within  the  province  of  the  specialist  rather  than  of 
the  general  practitioner,  and  I  shall  invite  your  attention 
only  to  the  more  prominent  points  in  their  history. 

TJlcerations  of  the  larynx  rarely,  if  ever,  are  met  with  as 
primary  aifections.  The  different  forms  of  laryngeal  ulcer- 
ations  are  included  under  the  following  heads  : — the  catarrh- 
al, the  follicular,  variolous,  typhous,  phthisical,  and  syphi- 
litic. The  most  common  forms  are  those  caused  by 
phthisis  or  syphilis. 

MORBID  ANATOMY. — Catarrhal  ulcers  are  usually  super- 
ficial, and  at  first  may  have  either  a  rounded  or  elongated 
shape  ;  afterwards,  as  the  loss  of  substance  is  more  extensive, 
they  coalesce  and  have  an  irregular  outline.  The  follicular 


24  ULCEllS   OF  THE    LARYNX. 

ulcers  are  always  circular  and  increase  in  depth  rather  than 
in  width.  These  two  forms  of  ulcers  never  lead  to  disease 
of  the  cartilages,  unless  they  occur  in  connection  with  pul- 
monary phthisis. 

They  may  be  situated  upon  any  portion  of  the  laryngeal 
membrane  ;  when  they  are  situated  upon  the  anterior  or  pos- 
terior ends  of  the  vocal  bands,  they  have  a  tendency  to 
spread  lengthwise. 

Variolous  ulcers  are  the  result  of  small-pox  pustules  on 
the  laryngeal  membrane.  They  commence  by  the  forma- 
tion of  soft  non-umbiiicated  pustules,  which  after  a  little 
burst  and  form  a  rounded  ulcer,  which  readily  heals. 

Typhous  ulcers  are  generally  of  large  size,  and  deep,  pene- 
trating through  the  mucous  membrane,  and  sometimes  in- 
volving the  cartilages.  The  edges  of  these  ulcers  are 
everted,  and  of  a  dark  purple  color  ;  their  most  common 
seat  is  the  posterior  wall  of  the  larynx,  and  the  edges  of  the 
epiglottis. 

Phthisical  ulcers. — The  most  frequent  seat  of  these 
ulcers  is  that  portion  of  the  laryngeal  membrane  covering 
the  posterior  surface  of  the  epiglottis  and  the  transverse 
muscles  of  the  larynx.  They  do  not  always,  if  ever,  origi- 
nate in  tubercle, — they  commence  as  minute  circular  ulcers, 
the  tissues  around  them  being  infiltrated  with  small  cells. 
By  the  union  of  the  small  ulcers  large  irregular  ones  are 
produced, — sometimes  they  produce  deep  destruction  of  tis- 
sue. The  epiglottis  is  often  eroded  at  its  margin,  and  the 
cartilage  may  be  exposed  or  perforated.  Calcification,  as 
well  as  necrosis  of  the  laryngeal  cartilages,  occasionally  fol- 
lows phthisical  ulceration. 

Syphilitic  ulcers. — Syphilitic  ulcerations  of  the  larynx 
are  usually  met  with  among  the  tertiary  manifestations 
of  syphilis,  and  rarely  if  ever  occur  as  secondary  lesions  of 
the  disease.  These  tertiary  ulcers  frequently  begin  on  the 
epiglottis  and  spread  rapidly  ;  they  often  involve  the  mucous 
membrane  of  the  entire  larynx,  and  cause  great  destruction 
of  tissue.  They  have  an  irregular  outline,  with  everted  edges 
and  yellow  hue,  excavated  base,  and  at  times  present  a 
more  or  less  gangrenous  appearance.  In  some  cases  they 


ETIOLOGY.  25 

extend  from  the  pharynx.  They  may  originate  in  the  break- 
ing down  of  syphilitic  tubercle  or  gummata.  They  often 
heal  at  the  point  attacked,  while  the  ulceration  advances 
in  other  places ;  the  scars  which  result  from  the  healing 
of  the  ulcers  have  a  tendency  to  contract  and  narrow  the 
calibre  of  the  larynx.  The  papillary  growths  which  sur- 
round these  ulcers  are  especially  characteristic  of  their 
syphilitic  origin. 

ETIOLOGY. — Catarrhal  laryngeal  ulcers  are  rarely  the  re- 
sult of  acute  laryngeal  catarrh  ;  but,  as  I  have  already  men- 
tioned, are  of  not  unfrequent  occurrence  in  chronic  catarrh- 
al  laryngitis,  especially  that  which  accompanies  pulmo- 
nary phthisis.  The  f ollicular  variety  generally  results  from 
the  extension  of  a  f  ollicular  faucitis  from  the  pharynx  to  the 
larynx,  or  at  least  the  two  are  frequently  associated. 

Variolous  ulcers  have  their  origin  from  the  propagation 
of  the  exanthema  from  the  mouth  and  pharynx. 

Typhous  ulcers  have  their  origin  either  in  diphtheritic 
infiltration  or  imperfect  nutrition  of  the  mucous  membrane 
of  the  larynx. 

Syphilitic  ulcers  depend  upon  a  specific  constitutional 
poison  acting  in  conjunction  with  a  catarrhal  inflammation 
of  the  mucous  membrane  of  the  larynx. 

Phthisical  ulcers  are  always  secondary  to  pulmonary 
phthisis,  and  as  a  rule  are  the  result  of  diffuse  degeneration 
of  the  mucous  membrane  of  the  larynx,  which  is  preceded 
and  accompanied  by  a  chronic  catarrh  of  the  larynx  ;  in 
some  instances  these  ulcers  may  be  tubercular,  but  generally 
they  are  of  catarrhal  origin. 

SYMPTOMS. — All  the  forms  of  laryngeal  ulcers  to  which  I 
have  referred  are  attended  by  the  general  symptoms  of 
chronic  laryngeal  catarrh.  When  a  patient  with  a  harsh, 
stridulous  cough  of  long  standing  (the  expectoration  con- 
taining pure  blood  and  laryngeal  tissue),  with  hoarseness  at 
times  amounting  to  aphonia,  complains  of  a  burning, 
smarting,  pricking  sensation  in  the  larynx,  with  tenderness 
on  pressure,  which  is  increased  by  speaking,  and  of  a  diffi- 
cult and  painful  deglutition,  with  a  wavy  laryngeal  respira- 
tion, we  have  reason  to  suspect  the  existence  of  a  laryngeal 


26  ULCERS    OF  THE   LARYXX. 

ulcer,  though  a  positive  diagnosis  cannot  be  made  from 
these  symptoms  alone,  as  extensive  ulceration  may  exist 
and  all  of  these  symptoms  be  wanting,  and  they  may  be 
present  where  there  is  only  simple  laryngeal  catarrh  without 
ulceration.  The  appearance  of  the  posterior  wall  of  the 
pharynx  is  always  of  great  diagnostic  importance. 

The  use  of  the  laryngoscope  clears  up  all  doubts  as  to  the 
existence  or  non-existence  of  laryngeal  ulcers.  By  a  care- 
ful laryngoscopic  examination  you  will  not  only  be  able  to 
determine  the  existence  of  these  ulcers,  but  also  their  seat 
and  extent.  Having  determined  their  existence,  the  history 
of  the  patient  and  a  careful  auscultatory  examination  of 
the  chest  will  enable  you  to  decide  as  to  the  character  of 
the  ulceration. 

PROGNOSIS.— The  prognosis  in  this  class  of  affections 
depends  entirely  upon  their  character.  The  catarrhal,  f  olli- 
cular,  typhous,  and  variolous  are  usually  amenable  to  treat- 
ment and  readily  recovered  from  ;  while  the  phthisical  and 
syphilitic  are  rarely  if  ever  entirely  healed,  or,  if  healed,  the 
destruction  of  the  parts  is  so  great  that  the  remaining  cica- 
trix  permanently  interferes  with  the  functions  of  the  larynx. 

TREATMENT.— The  treatment  of  laryngeal  ulcer  is  identi- 
cal with  that  of  chronic  catarrhal  laryngitis,  which  I  have 
already  sufficiently  considered. 


LECTURE    III. 


DISEASES  OP  THE  LARYNX 

Laryngeal  Paralysis. — Spasmodic   Affections   of  the  Larynx. — Pathological 
New  Formations  in  the  Larynx. 

I  SHALL  this  morning  continue  the  history  of  laryngeal 
affections  by  inviting  your  attention  to  its  functional  dis- 
turbances, or  neuroses  of  the  larynx. 

Sometimes  the  development  of  this  class  of  affections  oc- 
curs without  any  recognizable  organic  lesions ;  at  other 
times  they  are  symptomatic  of  local  or  distinct  organic 
disease. 

The  symptomatic  nervous  affections  of  the  larynx  are 
usually  more  lasting  and  serious  in  their  nature;  in  this 
latter  class  I  shall  include  laryngeal  paralysis. 

In  the  majority  of  cases  of  laryngeal  paralysis,  the  spinal 
or  recurrent  nerve  is  diseased,  or  subjected  to  pressure. 

LARYNGEAL  PARALYSIS. 

Paralysis  of  the  muscles  of  the  vocal  bands  may  be  divided 
as  follows : 

First, — paralysis  of  the  adductors  of  the  vocal  bands. 

Second^ — paralysis  of  the  abductors  of  the  vocal  bands. 

Third) — paralysis  of  the  tensors  of  the  vocal  bands. 

Each  form  of  paralysis  may  be  limited  to  one  side,  or  may 
affect  both  sides  of  the  larynx.  Frequently  two  kinds  of 
paralysis  are  present  in  the  same  individual,  and  affect  the 
same  or  different  muscles ;  rarely  is  only  a  single  muscle 
affected. 


LARYXGEAL   PARALYSIS. 

MORBID  ANATOMY.— In  many  instances  of  bilateral  paral- 
ysis of  the  adductors  of  the  vocal  bands  or  closures  of  the 
rinia  glottidis,  you  will  be  unable  to  detect  any  morbid 
change  in  the  tissues  which  compose  the  larynx  ;  frequently, 
however,  you  will  find  a  catarrha!  condition  of  the  laryngeal 
mucous  membrane,  which  will  be  congested  and  thickened, 
and  the  vocal  bands  wiU  have  lost  their  pearly  lustre  ;  such 
conditions  are  most  likely  to  be  met  with  in  the  second  and 
third  stages  of  pulmonary  phthisis.  In  the  absence  of  all 
morbid  appearances,  we  are  obliged  to  attribute  bilateral 
paralysis  of  the  vocal  bands  to  insufficient  or  unequal  supply 
of  generated  nerve-force. 

In  unilateral  paralysis  of  the  adductors  of  a  vocal  band, 
usually  one  of  the  recurrent  nerves  is  diseased,  either  pri- 
marily or  secondarily,  or  an  inflammatory  degenerative  pro- 
cess may  have  been  established  in  the  muscle  involved. 
Unilateral  compression  of  the  recurrent  nerve  by  malignant 
tumors,  aneurism  of  the  aorta,  innominata,  or  subclavian 
arteries,  as  well  as  degenerative  processes  in  the  nerve  itself, 
have  brought  about  this  form  of  paralysis.  Pathological 
changes  at  the  apices  of  the  lungs,  or  in  the  lymph  glands 
in  contact  with  the  nerves,  may  also  give  rise  to  this  form  of 
paralysis.  Forms  of  cerebral  disease  which  give  rise  to  loss 
of  power  in  the  tongue  and  palate,  on  the  same  side  as  the 
affected  vocal  band,  are  occasioned  by  a  morbid  condition 
met  with  in  connection  with  this  form  of  laryngeal  paralysis. 

In  bilateral  paralysis  of  the  abductors  of  the  vocal  bands, 
or  openers  of  the  rima  glottidis,  you  may  find  advanced 
phthisical  changes  at  the  apices  of  both  lungs,  or  advanced 
atrophy  of  the  laryngeal  muscles,  which  is  evidently  depen- 
dent upon  interruption  of  nerve-force,  either  from  cerebral 
disease  or  local  pressure  of  the  vagi,  or  from  both  recurrent 
nerves. 

In  unilateral  paralysis  of  the  abductor  of  the  vocal  band, 
local  pressure  from  different  kinds  of  tumors  is  most  fre- 
quently met  with,  and  the  wasting  of  muscular  tissue  which 
attends  such  pressure  is  usually  limited  to  one  side. 

Paralysis  of  the  tensor  muscles  of  the  vocal  bands  indi- 
cates trouble  in  the  spinal  nerve.  This  condition  is  not,  as 


ETIOLOGY.  29 

is  frequently  stated,  that  of  functional  disturbance.  There 
may  be  organic  lesions  present,  such  as  follow  contusion  or 
laceration  of  nerve-tissue.  Atrophy  of  the  spinal  accessory 
nerves,  consecutive  to  compression  in  their  passage  through 
the  foramen  lacerum  posterius,  has  occasionally  been  met 
with. 

ETIOLOGY. — The  etiology  and  morbid  anatomy  of  laryn- 
geal  paralysis  is  so  closely  connected,  that  in  speaking  to 
you  of  the  causes  of  these  affections,  I  shall  necessarily 
repeat  much  that  I  have  said  in  regard  to  its  morbid  anat- 
omy. 

A  very  common  cause  of  laryngeal  paralysis  is  some  local 
organic  change  in  the  mucous  tissues  of  the  larynx,  either 
past  or  present.  Repeated  catarrhal  inflammations  of  the 
larynx  in  very  many  instances  are  manifestations  of  a  condi 
tion  which  gives  rise  to  partial  or  complete  laryngeal  paraly- 
sis. Women  rather  than  men  are  subject  to  this  form  of 
paralysis. 

Again,  pressure  on,  or  traction  of,  the  pneumogastric  or 
recurrent  nerves,  by  tumors,  enlarged  glands,  and  thoracic; 
aneurisms,  are  frequent  causes  of  laryngeal  paralysis. 

Diphtheria,  typhus  and  malarial  fevers,  and  other  acute 
blood  diseases  are  occasionally  followed  by  laryngeal  paral- 
ysis ;  under  these  circumstances  the  paralysis  is  undoubt- 
edly due  to  the  .direct  effects  of  the  special  poison  of  these 
diseases  upon  the  nerve-centres. 

The  action  of  certain  metallic  poisons,  such  as  lead, 
arsenic,  mercury,  etc.,  upon  the  larynx,  after  months  or 
years  of  exposure  to  their  poisonous  influence,  may  cause 
laryngeal  paralysis. 

Centric  diseases  in  the  brain  or  upper  portion  of  the 
spinal  cord  sometimes  cause  laryngeal  paralysis.  Whenever 
you  meet  with  bilateral  paralysis  of  the  abductors,  you 
may  look  for  its  cause  in  some  more  or  less  well-defined 
lesion  of  the  brain. 

In  rare  instances,  laryngeal  paralysis  may  be  due  to 
atrophy  and  degeneration  of  the  laryngeal  muscle,  and 
comes  on  without  any  assignable  cause. 

Temporary  laryngeal  paralysis,  occurring  in  connection 


30  LATTFXGEAL  PARALYSIS. 

with  hysterical  manifestations,  has  no  cause  save  the  erratic 
one  of  hysteria,  appearing  and  disappearing  without  any 
apparent  cause.  Mechanical  violence  not  unfrequently 
causes  paralysis  of  the  tensors  of  the  larynx,  as  when  a 
blow  is  struck,  or  there  is  a  fall  upon  some  projection ;  it 
also  may  occur  as  a  sequelae  of  too  loud,  too  frequent,  and 
too  prolonged  exercise  of  the  voice  in  public  speaking. 

SYMPTOMS. — I  shall  consider  separately  the  phenomena 
which  attend  the  different  forms  of  paralysis  ;  they  are  for 
the  most  part  local  in  character. 

In  bilateral  paralysis  of  the  adductors,  the  loss  of  voice  is 
complete,  but  coughing  is  usually  attended  with  sound  of  a 
hoarse,  stridulous  character.  When  this  form  of  paralysis 
is  of  hysterical  origin,  the  voice  comes  and  goes,  at  times 
most  capriciously, — now,  it  is  normal,  and  in  a  short  time 
the  patient  may  become  completely  aphonic  without  any 
apparent  cause.  A  laryngoscopic  examination  of  the 
larynx  will  show  that  during  attempted  phonation  the 
vocal  cords  remain  apart ;  they  may  be  perfectly  motionless. 

In  unilateral  paralysis  of  the  adductors  usually  there  is 
dysphonia.  In  rare  instances  the  voice  will  be  unchanged, 
during  ordinary  conversation,  and  will  only  be  impaired 
when  an  endeavor  is  made  to  sound  the  higher  notes  in  sing- 
ing, or  after  some  extraordinary  continued  effort  of  the 
vocal  organs.  The  sound  produced  during  coughing,  sneez- 
ing, and  laughing,  is  usually  much  changed  and  weakened. 
The  laryngoscope  shows  that  one  vocal  band  is  or  is  not 
congested,  but,  at  all  events,  it  does  not  act  when  the  pa- 
tient attempts  to  speak  or  cough.  As  has  already  been 
stated,  this  form  of  paralysis  is  due  to  some  direct  cause 
acting  on  the  nerve  of  the  affected  side. 

Bilateral  paralysis  of  abductors  is  often  accompanied  by 
decided  hoarseness  and  huskiness  of  the  voice,  rarely  by  en- 
tire loss  of  voice  ;  articulate  speech  is  often  almost  normal, 
and  then  suddenly,  as  though  the  current  of  air  were  inter- 
rupted, the  patient  is  unable  to  make  himself  understood, 
so  feeble,  so  utterly  lost  has  his  phonetic  power  become. 

The  prominent  symptom  of  this  form  of  paralysis  is  dysp- 
ncea,  with  noisy,  stridulous  inspiration,  which  is  always 


DIFFERENTIAL  DIAGNOSIS. 

more  or  less  marked,  but  becomes  greatly  aggravated  after 
violent  exertion  or  on  deep  inspiration. 

A  laryngoscopic  examination  shows  both  vocal  bands  in 
juxtaposition,  near  the  median  line,  and  they  do  not  sepa- 
rate when  a  full  inspiration  is  made ;  on  the  contrary,  a 
forced  inspiration  makes  them  approach  even  to  touching, 
while  a  forced  expiration  separates  them  a  little. 

In  unilateral  abductor  paralysis,  the  voice  is  shrill  and 
discordant,  and  dyspnoea  is  present  only  after  physical 
exertion  ;  then  there  is  more  or  less  complete  aphonia.  Du- 
ring inspiration  the  paralyzed  band  does  not  move,  but  its 
edge  is  concave.  It  frequently  remains  stationary,  even 
when  not  in  the  median  line,  but  usually  it  remains  in  the 
median  line,  on  account  of  the  contraction  or  spasm  of  the 
adductors.  The  band  seems  shorter  than  normal,  and  usu- 
ally is  congested,  especially  after  attacks  of  dyspnoea. 

Generally,  there  is  no  difficulty  in  deglutition  in  any  of 
the  forms  of  laryngeal  paralysis  which  we  have  been  con- 
sidering ;  in  those  where  the  bands  do  not  approximate  suf- 
ficiently, there  may  be  slight  dysphagia. 

DIFFERENTIAL  DIAGNOSIS. — Laryngeal  paralysis  is  easily 
recognized  when  a  careful  laryngoscopical  examination  of  the 
larynx  is  made.  The  character  of  the  respiration  in  paral- 
ysis of  the  adductors,  and  that  in  paralysis  of  the  abduc- 
tors, is  usually  sufficiently  marked  to  distinguish  the  one 
from  the  other. 

In  adductor  paralysis,  the  respiration  is  always  per- 
formed with  ease  ;  while  in  paralysis  of  the  abductors,  dysp- 
noea and  stridulous  breathing  are  always  present  in  a 
greater  or  less  degree.  In  other  forms  of  laryngeal  paral- 
ysis the  respiration  is  normal. 

PROGNOSIS. — In  those  cases  where  paralysis  of  the  vocal 
bands  depends  upon  a  morbid  condition  of  the  nerve-cen- 
tres, or  is  due  to  compression  of  the  nerves  by  aneurisms  or 
new  formations,  the  prognosis  is  always  grave.  On  the 
other  hand,  it  is  favorable  when  it  is  due  to  functional 
causes,  or  originates  in  catarrhal  inflammation  of  the  mu- 
cous lining  of  the  vocal  organs.  When  there  is  paralysis  of 
the  adductors,  usually  the  prognosis  is  favorable ;  while 


32  LARYXGEAL   PARALYSIS. 

with  paralysis  of  the  abductors  the  patient  is  always  in 
great  danger. 

TREATMENT. — In  paralysis  of  the  adductors  and  tensors  of 
the  larynx,  where  any  method  of  treatment  can  be  of  ser- 
vice, the  surest  and  best  is  to  be  found  in  the  application  of 
the  electric  current,  galvanic  or  faradic,  one  pole  being 
placed  over  the  thyroid  or  cricoid  cartilage,  and  the  other 
in  contact  with  the  vocal  bands.  These  applications  must 
be  employed  at  regular  intervals,  and  only  for  a  short  period 
at  any  one  time. 

As  adjuvants,  stimulating  inhalations  may  be  employed, 
such  as  ammonia,  creosote,  etc.,  and  local  applications  of 
iron,  nitrate  of  silver,  etc. 

Whenever  the  abductor  muscles  have  lost  power,  it  becomes 
a  question  whether  tracheotomy  shall  or  shall  not  be  per- 
formed ;  if  the  dyspnoea  becomes  so  intense  as  to  be  a  source 
of  immediate  danger  to  the  patient,  tracheotomy  should  be 
performed  without  delay,  for  it  aifords  the  only  chance  of 
prolonging  life. 

Rest  of  the  voice  is  an  all-important  element  of  treatment, 
where  there  is  deficient  action  of  the  muscles  ;  and  in  obsti- 
nate cases,  electricity,  with  the  induced  or  galvanic  current, 
may  be  used  with  advantage  to  the  patient. 

In  all  forms  of  laryngeal  paralysis,  general  treatment  is 
often  indicated. 

SPASMODIC  AFFECTIONS  OF  THE  LARYNX. 

The  only  spasmodic  affection  of  the  larynx  of  which  I 
shall  speak  is  the  common  form  known  as  spasm  of  the  glot- 
tis or  laryngismus  stridulus,  which  is  occasioned  by  tem- 
porary spasm  of  the  adductors  of  the  larynx ;  this  gives 
rise  to  temporary  paroxysms  of  dyspnoea  and  stridulous 
breathing. 

MORBID  ANATOMY. — There  are  various  opinions  in  regard 
to  the  pathological  nature  of  spasms  of  the  glottis.  Ac- 
cording to  some  eminent  authorities,  there  exists  an  altered 
or  abnormal  condition  of  the  nerve-centres, — especially  is  this 
the  case  in  children, — while  other  authorities  recognize  an 
excessive  susceptibility  of  the  glottic  nerves  to  receive  reflex 


ETIOLOGY.  33 

impressions.  For  the  present,  I  shall  regard  spasm  of  the 
glottis  or  laryngismus  stridulus  as  a  spasmodic  affection 
of  the  purest  type  ;  in  severe  cases,  the  spasmodic  condition 
is  manifested  simultaneously  in  many  organs  of  the  body. 

When  an  adult  is  affected,  there  is  frequently  some  ca- 
tarrhal  or  inflammatory  condition  of  the  mucous  membrane 
of  the  larynx,  which  acts  as  an  efficient  cause  of  the  spasm  ; 
in  children,  usually  the  muco-lining  of  the  larynx  is  per- 
fectly healthy.  In  adults,  the  brain  is  normal  in  appear- 
ance ;  in  children,  serous  effusion  is  frequently  found  in  the 
ventricles  and  on  the  surface  of  the  brain.  Evidences  of 
rickets  are  frequently  apparent  in  the  osseous  system  of 
children  subject  to  laryngismus. 

The  condition  of  the  pneumogastric  nerve  has  been  vari- 
ously reported  by  those  who  have  written  on  this  subject. 
Unquestionably,  reflex  irritation  in  the  larynx  may  arise 
from  a  great  variety  of  causes. 

In  spasm  of  the  tensors  of  the  vocal  bands,  there  probably 
exists  a  morbid  condition  of  the  sympathetic  ganglia,  al- 
though this  is  by  no  means  an  established  fact. 

ETIOLOGY. — There  can  be  little  doubt  but  that  spasm  of 
the  glottis  is  usually  due  to  some  form  of  irritation  conveyed 
to  the  laryngeal  nerves.  The  seat  of  the  irritation  may  be 
in  the  brain,  along  the  course  of  the  nerves,  or  it  may  have 
a  reflex  origin. 

Laryngeal  spasm  is  most  frequently  met  with  in  children, 
when  indigestion,  teething,  and  impressions  of  external  cold 
are  usually  assigned  as  causes,  yet  in  most  cases  of  this 
class,  cerebral  irritation,  due  to  some  other  cause,  already 
exists.  Scrofulous  and  rachitic  children  are  said  to  be  es- 
pecially subject  to  spasm  of  the  glottis. 

In  adults,  it  is  observed  in  connection  with  hysterical 
manifestations,  and  is  sometimes  the  result  of  pressure  on 
the  nerves  ;  it  also  occurs  in  connection  with  irritation  from 
foreign  bodies.  It  has  been  met  with  as  a  sequelae  of  whoop- 
ing-cough. 

SYMPTOMS. — In  children,  the  laryngeal  spasm  usually 
comes  on  at  night,  during  sleep.  (As  I  have  already  de- 
scribed it  under  the  head  of  croup,  I  will  speak  only  of  those 


34  SPASMODIC   AFFECTIONS   OF   THE   LARYNX. 

things  demanding  special  attention.)  The  dyspnoea  attend- 
ing it  is  often  intense,  the  respirations  are  stridulous  and 
crowing  in  character,  and  the  child  presents  the  appearance 
of  extreme  apnoaa.  It  is  sometimes  attended  by  general 
convulsions,  in  which  there  is  extreme  contraction  of  the 
flexor  muscles  of  the  extremities.  Strabismus  and  involun- 
tary discharge  of  faeces  and  urine  are  sometimes  present. 
The  spasm  usually  subsides  suddenly,  the  recovery  is  com- 
plete, and  is  never  accompanied  or  followed  by  fever.  One 
of  the  characteristics  of  this  affection  is  the  tendency  to  re- 
currence of  the  attacks.  Death  from  suffocation  during  the 
paroxysm  may  occur,  but  it  is  exceedingly  rare. 

In  adults,  spasmodic  affection  of  the  larynx  is  either  hys- 
terical in  its  nature  or  it  depends  upon  interrupted  pressure 
along  the  course  of  the  recurrent  nerves.  It  gives  rise  to 
symptoms  similar  to  those  already  described,  except  that 
the  paroxysms  are  less  severe  and  are  more  persistent. 

DIFFERENTIAL  DIAGNOSIS. — The  only  disease  liable  to  be 
mistaken  for  the  one  under  consideration  is  croup,  and  I 
have  already  considered  its  diagnosis  under  that  head. 

PROGNOSIS. — Those  cases  which  depend  upon  reflex  causes 
generally  recover.  The  prognosis  in  every  case  will  depend, 
however,  upon  the  violence  and  frequency  of  the  spasm,  the 
age  of  the  patient,  and  above  all  upon  the  cause  of  the 
spasm  ;  a  spasm  of  the  glottis  depending  upon  interrupted 
pressure  of  an  aneurism  on  the  recurrent  nerve,  not  unfre- 
quently  is  the  immediate  cause  of  death. 

TREATMENT. — If  spasm  of  the  glottis  is  due  to  reflex  irri- 
tation, you  must  immediately  seek  for  the  cause  of  the 
irritation,  and  remove  it.  In  children,  an  overloaded  stom- 
ach or  dentition  is  most  frequently  the  source  of  the  irri- 
tation. In  prolonged  attacks,  inhalation  of  ether  or  chloro- 
form may  be  tried,  or  a  hot  bath,  or  an  emetic  may  be 
promptly  administered. 

During  the  interval  between  the  paroxysms  careful  atten- 
tion must  be  paid  to  the  diet  and  general  hygiene  of  the 
patient.  If  the  spasms  are  severe  and  prolonged,  and  the 
patient  seems  to  be  sinking  from  the  apnoea,  the  trachea 
must  be  opened  and  artificial  respiration  resorted  to. 


MORBID   ANATOMY.  35 

When  laiyngismus  occurs  in  the  adult,  those  means  which 
have  been  found  serviceable  for  children  may  be  employed 
for  its  relief. 

When  laryngeal  spasm  occurs  as  a  hysterical  phenome- 
non, it  must  be  treated  in  the  same  manner  as  any  other 
hysterical  symptom. 

If  it  occurs  in  connection  with  pressure  upon  any  portion 
of  the  pneumogastric  nerve,  you  must  be  prepared  at  any 
moment  to  perform  tracheotomy  for  temporary  relief. 

Before  leaving  the  nervous  affections  of  the  larynx  it 
remains  for  me  to  say  a  few  words  on  changes  in  the  sensory 
system  of  the  larynx. 

The  sensibility  of  this  organ  may  be  increased,  diminish- 
ed, or  perverted. 

Hyper cEstliesicb  may  and  does  frequently  accompany  in- 
flammatory diseases  situated  in  this  region.  It  is  also  not 
unfrequently  found  in  females  suffering  from  hysteria  in 
connection  with  other  evidences  of  extreme  nervous  disturb- 
ance. In  these  cases,  no  organic  lesion  can  be  found,  and 
the  hypersesthesia  must  be  regarded  as  purely  functional. 

Anesthesia  of  the  larynx  is  met  with  in  cedematous  con- 
ditions of  the  posterior  wall  of  the  pharynx  in  laryngeal 
phthisis,  and  in  connection  with  an  abnormal  condition  of 
the  superior  laryngeal  branches  of  the  pneumogastric  nerve. 

These  abnormal  conditions  in  the  sensibility  of  the  larynx 
have  no  clinical  importance,  and  I  shall  not  detain  you  with 
their  fuller  history,  but  will  pass  on  to  our  next  subject. 

PATHOLOGICAL  NEW  FORMATIONS  IN  THE  LARYNX. 

Under  this  head  I  shall  speak  briefly  of  those  accidental 
productions  which  appear  as  tumors,  or  projections  on  the 
mucous  membrane  of  the  larynx,  and  which  interfere  more 
or  less  with  the  integrity  of  the  vocal  organs.  Laryngeal 
growths  may  be  divided  into  two  general  classes,  benign 
and  malignant. 

In  the  estimation  of  some  authorities,  there  is  more  than 
one  exception  to  this  division ;  as,  for  instance,  the  sarco- 
mata may  be  considered  as  resting  on  the  confines  of  the 
malignant  and  benign  growths.  These,  with  other  neoplasms 


36       PATHOLOGICAL   XEW   FORMATIONS   1JNT  THE   LAEYXX. 

of  a  mucous  tissue,  have  a  clinical  history  which  would  fully 
characterize  them  as  malignant,  and  yet  under  the  micro- 
scope we  are  unable  to  find  the  structure  of  malignant 
growth.  The  converse  of  this  may  also  be  true. 

MORBID  ANATOMY. — I  shall  only  briefly  consider  the 
morbid  anatomy  of  those  laryngeal  growths,  with  which  you 
should  be  familiar  on  account  of  their  frequency  ;  other  forms 
are  more  especially  interesting  on  account  of  their  rarity. 

Morbid  growths,  as  they  occur  in  the  larynx,  may  have  a 
broad  base  which  attaches  itself  to  the  interior  lining  mem- 
brane of  the  larynx,  or  they  may  hang  as  it  were  into  the 
interior  of  the  larynx  from  a  narrow  neck  or  peduncle. 
They  may  vary  in  size,  in  shape,  in  consistenc}^,  and  in 
number.  They  may  fill  up  the  cavity  of  the  larynx,  so  as 
to  impair  respiration,  or  they  may  be  of  such  small  size  as 
to  pass  unnoticed.  Three-fifths  of  all  the  benign  growths 
which  occur  in  the  larynx  are  papillomata;  where  these 
growths  are  congenital,  the  proportion  is  even  greater. 
These  tumors  grow  rapidly ;  sometimes  they  attain  a  con- 
siderable size  in  the  space  of  a  few  months. 

For  the  most  part,  their  structure  is  similar  to  that  of  the 
normal  papillae.  Their  basic  substance  is  formed  of  con- 
nective tissue,  which  receives  into  its  interior,  vessels  and 
nerves,  while  the  surface  is  covered  by  more  than  one  layer 
of  epithelium.  They  have  decidedly  a  villous  appearance ; 
some  of  these  growths  contain  spaces  filled  with  colloid 
matter  ;  after  removal,  they  are  quite  likely  to  again  make 
their  appearance. 

Relations  have  been  traced  between  benign  papillary 
growths  and  warty  cancers.  Some  cases  are  related  where 
papillomata  have  become  softened,  fatty,  and  cheesy,  and 
have  been  removed  by  coughing  ;  under  such  circumstances, 
spontaneous  cure  was  the  result. 

Fibromata  are  of  less  frequent  occurrence  than  papillo- 
mata ;  they  grow  less  rapidly,  and  are  never  congenital. 
These  growths  are  composed  of  white  fibres,  diverging  and 
interlacing  one  another  in  different  directions  ;  after  re- 
moval they  do  not  return.  They  are  generally  smooth, 
rounded,  pedunculated,  and  vascular. 


ETIOLOGY.  87 

Fibro-cellular  growths  are  composed  of  fibro-cellular  tis- 
sue. They  usually  contain  a  serous  fluid,  are  slow  of  growth, 
single,  and  after  removal  show  no  disposition  to  return. 

Cystic  tumors  are  due  to  enlargement  of  the  glands  in  the 
mucous  membrane.  They  contain  a  white,  sebaceous-like 
material,  and  have  thick  walls.  This  variety  of  tumor  is 
less  frequently  met  with  than  any  of  the  other  varieties. 

Glandular  growths  take  their  origin  in  the  larynx,  where 
the  glands  and  follicles  are  most  abundant.  They  may 
attain  to  great  size,  and  their  volume  is  much  influenced  by 
laryngeal  catarrh. 

These  mucous  growths,  fatty  or  vascular  tumors,  are  ex- 
ceedingly rare  in  the  larynx.  Laryngeal  growths  may  be 
and  frequently  are  of  complex  structure  ;  under  such  cir- 
cumstances, they  should  be  named  according  to  their  pre- 
dominating elements. 

Carcinomatous  growths  in  the  larynx  are  of  two  varieties, 
epithelial  and  medullary.  The  epithelial  form  is  most  fre- 
quent. The  medullary  is  not  so  liable  to  ulcerate  as  is  the 
epithelial,  but  produces  more  displacement.  Sometimes 
profuse  hemorrhage  occurs  in  connection  with  epithelial 
cancer  of  the  larynx. 

ETIOLOGY  OF  LAEYJSTGEAL  GROWTHS.  —The  most  frequent 
cause  of  laryngeal  growths  unquestionably  is  chronic  or 
frequently  recurring  laryngitis.  In  some  cases  a  more  or 
less  constant  irritation  of  the  vocal  organs  seems  to  give 
rise  to  their  development,  such  as  is  met  with  among  teach- 
ers, orators,  etc. 

Around  the  ulcerations  of  syphilis,  or  those  due  to  so- 
called  laryngeal  phthisis,  we  find  these  growths  spring  up 
most  readily. 

Those  whose  calling  subjects  them  constantly  to  the  in- 
halation of  irritating  vapors  or  dust,  are  especially  liable 
to  laryngeal  growths. 

Non-malignant  tumors  of  the  larynx  are  always  associ- 
ated in  their  origin  with  local  hypersemia.  In  malignant 
growths,  in  addition  to  the  local  changes,  there  are  consti- 
tutional influences  in  operation  which  impart  to  them  a 
specific  character. 


38  LARYXGEAL   GROWTHS. 

Laryngeal  growths  are  sometimes  congenital. 

SYMPTOMS. — The  symptoms  that  attend  laryngeal  growths 
are  for  the  most  part  local  in  character,  and  these  local 
symptoms  will  necessarily  vary  with  the  size,  situation,  and 
nature  of  these  morbid  growths,  as  well  as  with  the  size  of 
the  larynx. 

The  development  of  these  tumors  is  rarely  accompanied  by 
pain,  but  sometimes  there  is  a  sense  of  uneasiness,  as  though 
a  foreign  mass  were  in  the  larynx. 

Respiration  may  be  more  or  less  interfered  with  ;  thus  we 
may  have  more  or  less  dyspnoea,  but  usually  it  is  present 
only  after  somewhat  violent  physical  exertion,  such  as  run- 
ning, jumping,  going  up  a  long  flight  of  stairs,  etc.  The 
breathing  is  sometimes  stridulous  in  character  and  frequent. 
Suffocative  attacks  may  come  on,  which  are  due  to  spasm. 
When  the  growth  is  above  the  glottis,  all  the  difficulty  in 
breathing  is  on  inspiration  ;  the  expiration  is  quite  free. 

The  voice  is  always  more  or  less  changed  ;  it  is  not  only 
altered  in  quality,  and  liable  to  sudden  changes  in  intensity, 
but  sometimes  it  is  completely  lost. 

Cough  is  present  in  many  cases,  usually  it  is  a  mere  ap- 
pendage to  the  accompanying  laryngitis  ;  not  unfrequently 
it  is  voluntarily  excited  with  desire  on  the  part  of  the  pa- 
tient to  get  rid  of  the  laryngeal  obstruction.  In  the  expec- 
toration, which  is  usually  increased  by  coughing,  fragments 
of  the  growth  are  sometimes  found  ;  usually  there  is  nothing 
which  can  be  considered  as  distinctive  about  it. 

Dysphagia  is  present  in  the  advanced  stages  of  many 
laryngeal  growths,  especially  when  they  are  of  a  malignant 
type. 

The  most  positive  evidences  of  laryngeal  growths  are  fur- 
nished by  laryngoscopic  examinations. 

By  a  moderately  expert  laryngoscopic  examination  of  the 
interior  of  the  larynx,  you  will  not  only  be  able  to  recog- 
nize the  existence  of  the  laryngeal  growths,  but  to  determine 
their  seat  and  size,  and  in  some  cases  their  nature. 

DIFFERENTIAL  DIAGNOSIS. — The  interference  with  the 
functions  of  the  larynx  will  direct  your  attention  to  this 
organ  as  the  seat  of  disease,  and  when  you  employ  the 


TREATMENT.  39 

laryngoscope,  rarely  if  ever  will  you  overlook  the  existence 
of  these  growths  ;  when  seen,  it  will  hardly  be  possible  to 
confound  them  with  any  other  disease,  and  you  will  be 
assisted  in  making  a  differential  diagnosis  by  carefully 
studying  the  histories  of  such  cases  as  are  recorded  in 
laryngoscopic  manuals. 

PROGNOSIS. — This  may  be'  considered  as  regards  loss  of 
function,  and  as  regards  loss  of  voice.  If  the  growth  be 
pedunculated,  of  moderate  size  and  single,  with  ordinary 
condition  of  tolerance,  in  many  instances  the  voice  can  be 
entirely  restored.  If  the  contrary  condition  exists,  relief  may 
be  looked  for,  but  never  complete  restoration  of  the  voice. 

As  to  length  of  life,  other  things  being  equal,  the  progno- 
sis is  more  favorable  in  regard  to  adults  than  to  children, 
for  the  reason  that  evulsion  of  the  growth  by  the  intra-la- 
ry  iigral  methods  is  more  readily  and  certainly  accomplished 
in  the  former  than  in  the  latter. 

Whenever  these  growths  are  cancerous  in  their  nature, 
they  terminate  fatally. 

TREATMENT. — If  a  laryngeal  growth  is  small,  and  does 
not  interfere  with  the  voice  or  respiration,  the  rule  is,  to  let 
it  alone ;  if,  on  the  other  hand,  it  is  of  considerable  size, 
and  is  increasing  rapidly,  endangering  life,  operative  meas- 
ures must  be  resorted  to,  either  intra-  or  extra-laryngeal  in 
character.  These  more  properly  fall  within  the  province  of 
the  specialist  than  of  the  general  practitioner. 

Whenever  there  is  great  obstruction  to  respiration,  and 
suffocation  seems  imminent,  tracheotomy  should  be  imme- 
diately performed,  after  which  the  intra-laryngeal  methods 
of  procedure  may  be  resorted  to. 

In  malignant  laryngeal  growths,  all  remedial  measures  are 
only  palliative  in  their  nature. 

Ossification  and  calcareous  infiltration  of  the  cartilages 
of  the  larynx  are  met  with  in  those  cases  where  there  has 
been  chronic  and  frequently  recurring  laryngitis  ;  not  unfre- 
quently  the  calcareous  condition  of  the  cartilage,  which  is 
sometimes  present  in  connection  with  chondritis  or  peri- 
chondritis,  is  preceded  by  its  ossification. 


LECTURE   IV. 


BRONCHITIS. 


Definition. — Acute  Catarrhal  Bronchitis  of  the  larger  Tubes. — Capillary  Bron- 
chitis. 


I  SHALL  this  morning  commence  the  history  of  bron- 
chitis. It  is  essentially  an  inflammation  of  the  mucous 
membrane  of  the  larynx,  trachea,  and  bronchial  tubes,  which 
may  vary  in  extent,  intensity,  and  duration.  Thus  it  may 
be  limited  to  the  larynx,  trachea,  and  larger  bronchi,  or  it 
may  extend  into  the  capillary  tubes ;  it  may  be  mild  or 
severe  in  character,  run  a  rapid  course  or  be  indefinitely 
protracted.  It  may  also  be  produced  by  a  variety  of 
causes,  some  external,  some  internal,  some  accidental,  and 
others  constitutional.  It  may  be  primary  or  secondary, 
— primary,  when  the  result  of  exposure,  or  produced  by  the 
inhalation  of  irritating  gases;  secondary,  when  it  arises 
from  some  constitutional  vice,  or  from  previously  existing 
disease.  Again,  it  may  occur  as  a  complication  during 
the  course  of  other  diseases,  such  as  acute  blood  disease, 
pulmonary  phthisis,  pulmonary  emphysema,  and  cardiac 
disease. 

Bronchitis,  clinically  and  pathologically,  may  be  divided 
into  the  following  varieties : 

First. — Acute  catarrhal  bronchitis,  which  may  be  simple 
or  capillary. 

Second. — Chronic  catarrhal  bronchitis,  which  generally  is 
a  secondary  affection. 


MOKBID   ANATOMY.  41 

Third. — Croupous  or  plastic  bronchitis  which,  may  be 
acute  or  chronic. 

ACUTE  CATARRHAL  BRONCHITIS. 

This  form  of  bronchial  inflammation  occurs  at  all  ages. 
In  childhood  and  old  age  it  most  frequently  involves  the 
smaller  bronchi ;  in  adult  life  it  involves  the  larger  bronchi. 
It  may  be  mild  or  severe  in  type. 

Morbid  Anatomy. — The  morbid  anatomy  of  this  variety 
of  bronchitis  does  not  differ  essentially,  whether  it  has  its 
seat  in  the  large  or  small  bronchial  tubes.  In  either  case,  it 
rarely  originates  in  the  tubes  themselves,  but  is  the  con- 
tinuation of  a  similar  process  affecting  the  nasal,  pharyngeal, 
and  laryngeal  mucous  membrane,  or  is  the  extension  to  the 
smaller  tubes  of  an  inflammation  commencing  in  the  alveoli. 
As  a  rule,  the  simple  variety  does  not  advance  beyond  the 
larger  bronchi ;  when  the  smaller  tubes  are  involved  it  is 
denominated  capillary.  In  some  cases  the  mucous  mem- 
brane is  swollen  and  reddened,  either  uniformly  or  in  points 
or  patches — it  is  softer  and  more  moist  than  natural — occa- 
sionally ecchymoses  are  observed  in  it.  The  bronchi  at  first 
contain  a  clear,  transparent  mucus,  which,  as  the  disease 
advances,  becomes  opaque,  whitish,  yellowish,  greenish,  or 
muco-purulent.  The  change  in  the  color  of  the  secretion  is 
owing  to  an  increase  in  the  number  of  the  cells  contained  in 
the  fluid  ;  at  the  onset  there  are  but  few  present.  The  cells 
are  pus-cells  and  ciliated  epithelium ;  the  presence  of  the 
latter  in  the  tubes  after  death  is  for  the  most  part  owing  to 
their  separation  from  the  membrane,  between  the  time  of 
death  and  the  making  of  the  autopsy. 

In  not  a  small  proportion  of  cases,  the  only  evidence  of 
bronchitis  which  you  will  find  on  post-mortem  examination 
is  the  presence  of  mucus  or  muco-pus  in  the  tubes. 

These  same  changes  exist  whether  the  larger  or  smaller 
tubes  are  the  seat  of  the  inflammation.  Generally  the  tubes 
on  both  sides  are  equally  affected.  In  some  instances,  only 
in  the  smaller  tubes  are  found  evidences  of  inflammation  ;  in 
other  instances,  only  in  the  larger  ones  ;  again,  they  will  be 
found  in  both. 


42  ACUTE  CATARRHAL  BRONCHITIS. 

In  the  weak,  the  very  young,  and  the  very  old,  or  when 
there  is  some  condition  which  prevents  or  enfeebles  the 
cough,  the  mucus  or  muco-pus  sometimes  gravitates  from  the 
larger  into  the  smaller  tubes,  and  gives  rise  to  yellow  spots 
near  the  surface  of  the  lung  ;  this  is  especially  liable  to  oc- 
cur in  young,  feeble  children. 

With  acute  bronchitis  we  sometimes  have  complications. 
The  swollen  mucous  membrane,  or  the  accumulation  of 
mucus  or  muco-pus  may  produce  a  temporary  obstruction 
in  the  smaller  tubes,  and  lead  to  a  temporary  air  distention 
of  the  alveoli, — a  condition  frequently  met  with  at  autopsies, 
and  sometimes  mistaken  for  vesicular  emphysema.  Fully 
developed  emphysema,  as  well  as  atelectasis,  may  occur  as 
the  result  of  these  bronchial  obstructions.  Occasionally,  in 
these  patches  of  collapsed  lung,  or  as  a  result  of  the  exten- 
sion of  inflammation  from  the  bronchi  to  the  alveoli,  lobular 
pneumonia  occurs, — this  is  rare  in  the  acute  bronchitis  of 
adults,  but  frequent  in  children. 

Pulmonary  congestion  and  oedema  is  not  unfrequently  a 
complication  of  general  capillary  bronchitis. 

Temporary  bronchial  dilatation  often  occurs  in  children 
when  the  disease  affects  the  smaller  tubes,  and  lasts  more 
than  a  week. 

Ulceration  of  the  mucous  membrane  of  the  trachea  or 
bronchi  very  rarely  occurs  in  acute  catarrhal  bronchitis. 
The  bronchial  glands  are  often  enlarged,  congested,  and 
softened. 

ETIOLOGY. — The  most  marked  predisposing  causes  of  acute 
bronchial  catarrh  are,  infancy  or  old  age,  indulgence  in 
enervating  habits,  or  debility  from  any  cause,  constitutional 
diseases,  chronic  pulmonary  affections,  the  breathing  of  im 
pure  air  in  badly  ventilated  apartments,  and  sudden  changes 
of  temperature. 

The  disease,  when  primary,  is  either  due  to  some  sudden  at- 
mospheric change,  to  some  morbific  agent  in  the  atmosphere, 
or  to  the  action  of  cold  on  the  surface  of  the  body  when  im- 
perfectly protected,  causing  a  chilling  of  the  surface.  It  oc- 
curs secondarily  in  connection  with  blood-poisoning,  as  in 
measles,  typhoid  and  typhus  fevers,  gout,  rheumatism,  etc. 


SYMPTOMS.  43 

In  the  course  of  other  pulmonary  affections,  and  in  chronic 
cardiac  disease,  it  is  of  qiiite  frequent  occurrence. 

It  may  be  produced  traumatically  by  the  inhalation  of 
irritating  gases,  particles  of  dust,  etc.,  which  act  directly 
upon  the  mucous  membrane,  causing  congestion  and  ca- 
tarrh. 

Those  who  live  in  the  open  air  are  less  liable  than  those 
living  in-doors  to  attacks  of  bronchitis. 

Lastly,  at  times  bronchitis  occurs  epidemically,  associated 
with  influenza  from  the  action  of  some  unknown  atmospheric 
influence. 

SYMPTOMS. — A  common  cold  may  be  regarded  as  a  bron- 
chitis of  the  larger  tubes.  This  simple  form  of  bronchial 
catarrh  does  not  extend  farther  down  than  the  second  di- 
vision of  the  bronchial  tubes,  but  expends  itself  on  the 
larynx,  trachea,  and  the  first  and  second  divisions  of  the 
bronchi. 

Its  invasion  is  commonly  marked  by  coryza,  sore  throat 
and  slight  hoarseness,  with  chilliness  scarcely  amounting  to 
rigor.  The  occurrence  of  the  coryza,  with  an  uneasy  sensa- 
tion in  the  frontal  sinuses,  gradually  passing  down  the  nasal 
passages  to  the  larynx  and  trachea,,  are  diagnostic  of  its  pri- 
mary character.  The  pulse  is  slightly  increased  in  force 
and  frequency, — there  is  aching  in  the  back  and  limbs, — the 
general  febrile  symptoms  are  usually  mild  ;  in  very  young 
and  weakly  children  convulsions  may  occur. 

As  the  bronchial  inflammation  becomes  fully  established, 
more  or  less  pain  and  discomfort  is  felt  behind  the  sternum  ; 
there  is  a  sense  of  rawness  and  soreness  at  the  upper  portion 
of  the  chest,  which  becomes  painful  on  coughing  ;  the  respi- 
rations are  somewhat  increased  in  frequency,  and  there  is  a 
sensation  of  constriction  and  oppressed  breathing — it  may  be 
somewhat  laborious,  but  there  is  no  evident  dyspnoea. 

The  cough,  an  essential  feature  of  the  disease,  at  first  is  dry 
and  hacking,  sometimes  incessant,  especially  on  lying  down 
and  on  waking  after  a  long  sleep  ;  it  may  be  paroxysmal  in 
character.  After  one  or  two  days  the  cough  becomes  loose, 
and  is  attended  with  an  expectoration  of  frothy  mucus,  of 
a  yellowish  color  and  a  saline  taste ;  gradually  this  becomes 


44  ACUTE    CATARRH AL   15ROXCIIITIS. 

muco-purulent  and  even  purulent.  Under  the  microscope, 
the  material  expectorated  will  be  found  composed  of  epithe- 
lial cells,  numerous  young  cells,  pus-cells,  with  abundant 
granular  and  molecular  matter,  a  few  blood-globules,  and 
fibrinous  coagula. 

As  soon  as  the  expectoration  becomes  free  the  patient  is 
relieved. 

The  disease  lasts  from  four  or  five  days  to  two  or  three 
weeks,  and  ends  in  complete  recovery  or  in  chronic  bron- 
chitis. 

PHYSICAL  SIGNS. — In  slight  attacks  of  acute  catarrhal 
bronchitis  of  the  larger  tubes,  there  may  be  no  physical 
signs  to  indicate  the  presence  of  the  inflammatory  action. 
The  severer  forms  are  attended  by  easily  recognized  physi- 
cal signs.  As  -a  rule,  inspection  and  palpation  give  nega- 
tive results,  and  the  percussion  sounds  are  normal,  unless 
there  is  a  very  considerable  accumulation  of  mucus  in  the 
bronchial  tubes ;  in  such  cases  the  normal  resonance  is  di- 
minished posteriorly  in  the  infra-scapular  region.  In  auscul- 
tation over  that  portion  of  lung  which  corresponds  to  the 
affected  tubes,  the  •  respiratory  murmur  is  feeble,  tempora- 
rily suppressed  or  sonorous  in  character.  In  the  dry  stage, 
sibilant  and  sonorous  rales  may  be  heard  on  both  sides  over 
the  whole  chest,  more  distinctly  heard  posteriorly.  In  the 
stage  of  secretion,  along  with  the  sibilant  and  sonorous  rales, 
moist  rales,  large  and  small  in  size,  are  heard  on  both  sides 
of  the  chest.  These  rales  are  inconstant,  coming  and  going, 
and  changing  their  situation  ;  after  a  violent  fit  of  coughing 
they  may  entirely  disappear  for  a  time.  When  they  are 
abundant  and  intense  they  often  altogether  mask  the  respi- 
ratory murmur.  In  some  cases  secretion  takes  place  so 
rapidly  that  moist  rales  are  heard  from  the  first.  In  cases 
of  slight  bronchitis  of  the  larger  tubes,  although  there  may 
be  no  distinct  rales,  the  respiration  will  often  have  a  distinct 
sonorous  character,  termed  sonorous  respiration. 

Vocal  resonance  in  bronchitis  is  normal. 

DIFFERENTIAL  DIAGNOSIS. — It  is  hardly  possible  to  con- 
found simple  bronchitis  with  any  other  pulmonary  affection. 
The  absence  of  lancinating  pains  in  either  side,  the  bronchial 


MORBID   ANATOMY.  45 

character  of  the  cough  and  expectoration,  the  coryza  and 
hoarseness  which  precede  the  attack,  are  usually  sufficient 
to  distinguish  it  from  pneumonia  and  pleurisy  ;  besides,  its 
physical  signs,  if  properly  appreciated,  render  the  diagnosis 
easy  and  positive  in  all  cases. 

PROGNOSIS. — This  form  of  bronchitis,  unless  it  occurs  in 
very  young  children,  never  directly  destroys  life. 

It  usually  terminates  by  resolution,  sometimes  it  becomes 
chronic  ;  in  such  cases  the  inflammation  is  likely  to  extend 
itself  into  some  of  the  smaller  tubes,  giving  rise  to  circum- 
scribed capillary  bronchitis  and  lobular  pneumonia. 

TREATMENT. — In  the  majority  of  cases,  this  form  of  bron- 
chitis is  easily  managed.  In  mild  attacks  the  patient  is  not 
sufficiently  ill  to  consult  a  physician  ;  it  is  simply  regarded 
as  a  severe  cold. 

At  the  onset,  while  the  coryza  is  present,  it  may  generally 
be  arrested  by  a  Dover's  powder  and  warm  bath  at  night, 
followed  in  the  morning  by  a  brisk  saline  purge, — in  the 
case  of  children  by  a  full  dose  of  castor-oil ;  the  patient 
should  remain  in  a  warm,  moist,  equable  temperature  for  a 
day  or  two.  If  this  plan  has  not  been  resorted  to,  or  has 
not  proved  successful,  then  moderate  but  continued  action 
of  the  skin  and  kidneys  should  be  induced  by  the  adminis- 
tration of  mild  diaphoretics  and  diuretics,  the  patient  re- 
maining in  a  warm,  equable  temperature. 

In  the  early  stage  of  the  disease,  especially  in  the  case  of 
children,  great  benefit  is  often  derived  from  the  inhalation 
of  the  vapor  of  molasses  and  water.  Counter-irritation  by 
means  of  cups,  of  mustard  sinapisms  to  the  upper  part  of 
the  chest,  are  of  great  service  in  the  later  as  well  as  in  the 
earlier  stages  of  the  disease.  If  the  disease  shows  a  ten- 
dency to  pass  into  the  chronic  stage,  or  to  extend  itself  into 
the  smaller  tubes,  from  eight  to  ten  grains  of  the  sul- 
phate of  quinine  should  be  daily  administered, — in 
children,  cod-liver  oil  with  lime-water  should  be  given. 
A  succession  of  small  blisters  applied  to  the  posterior 
portion  of  the  chest  will  be  of  service  after  the  acute  stage 
is  past. 

When  simple  bronchitis  occurs  in  persons  of  a  gouty  or 


46  ACUTE   CAPILLARY   BRONCHITIS. 

rheumatic  diathesis,  colchicum  must  be  given  in  connection 
with  alkalies. 

ACUTE  CAPILLARY  BRONCHITIS. 

As  I  have  already  stated,  when  acute  catarrhal  inflamma- 
tion invades  the  small -sized  bronchial  tubes,  it  is  termed 
capillary. 

In  most  instances,  this  form  is  an  extension  of  simple 
bronchitis,  preceded  by  similar  symptoms ;  but  sometimes 
the  smaller  as  well  as  the  larger  bronchial  tubes  are  affect- 
ed, or  they  may  be  the  primary  seat  of  the  inflammatory 
process. 

Capillary  bronchitis  is  much  more  frequently  met  with  in 
infancy  and  old  age  than  during  any  other  period  of  life. 

If  the  inflammation  is  limited,  and  only  a  few  of  the 
smaller  tubes  are  involved,  it  is  called  localized  capillary 
bronchitis  ;  but  when  the  bronchial  inflammation  is  intense 
and  diffused  over  the  lining  membrane  of  all  the  bronchial 
tubes,  it  is  termed  general  capillary  bronchitis. 

In  the  symptoms  which  attend  its  development,  and  in  its 
tendency  to  destroy  life,  it  differs  very  much  from  simple 
bronchitis. 

The  morbid  anatomy  of  this  form  of  bronchitis  has  been 
already  sufficiently  described ;  but  its  symptomatology, 
prognosis,  and  treatment  require  separate  consideration. 

The  causes  which  give  rise  to  capillary  bronchitis  are  sim- 
ilar to  those  which  I  have  named  in  connection  with  the 
etiology  of  simple  bronchitis,  except  in  those  instances 
where  it  occurs  as  a  secondary  affection.  The  danger  from 
acute  catarrhal  inflammation  of  the  smaller  tubes  in  pa- 
tients with  Bright' s  disease,  typhus  fever,  measles,  and  the 
chronic  bronchitis  of  old  age,  should  never  be  lost  sight  of. 

SYMPTOMS. — The  milder  types  of  this  form  of  bronchitis 
are  usually  preceded  by  inflammation  of  the  larger  tubes, 
and  the  symptoms  of  invasion  are  not  marked.  In  fact, 
the  capillary  element  of  the  disease  might  not  be  recognized 
were  it  not  for  the  physical  signs  and  difficult  or  labored 
respiration. 

On  the  other  hand,  the  severer  forms  may  be  ushered  in 


SYMPTOMS.  47 

by  distinct  drills,  high  febrile  excitement  and  great  dysp- 
noea. The  patient  is  unable  to  lie  down  on  account  of  the 
difficulty  of  breathing,  and  the  countenance  is  anxious  and 
flushed.  The  respirations  are  accelerated,  running  up  to 
60  or  70  in  a  minute,  attended  by  great  muscular  effort. 
The  pulse  is  feeble,  beating  from  100  to  130  in  a  minute. 
The  axillary  temperature  is  raised  to  103°  F.,  but  as  the 
disease  advances  it  may  fall  as  low  as  100°  F.,  although  the 
pulse  and  respiration  remain  frequent. 

The  patient,  at  the  commencement  of  the  attack,  has  an 
incessant  hacking  cough,  which  is  often  so  violent  as  to 
compel  the  patient  to  sit  up,  bend  forward,  and  hold  his 
sides.  At  first,  there  is  little  if  any  expectoration — if  any, 
it  is  a  thick  tenacious  mucus ;  later,  it  becomes  more 
abundant  and  less  tenacious.  The  cough  may  be  accom- 
panied by  a  rattling  sound  in  the  trachea.  There  is  great 
exhaustion.  If  the  disease  progresses,  all  the  phenomena 
of  deficient  oxygenation  are  developed. 

The  face  betokens  great  distress  and  has  a  livid  aspect, — 
the  lips  become  blue,  and  there  is  blueness  of  the  finger- 
ends,  with  fulness  of  the  jugular  veins.  The  respiratory 
acts  become  more  and  more  labored  and  imperfect,  the  ex- 
pectoration becomes  more  and  more  abundant,  and  the 
matter  expectorated  is  thin,  frothy,  and  tenacious.  There 
is  great  restlessness  and  signs  of  impending  suffocation,  the 
surface  of  the  body  is  covered  with  a  cold  clammy  sweat ; 
as  death  approaches  the  pulse  becomes  small  and  thready, 
the  respiratory  efforts  are  less  violent  and  less  frequent, 
— muttering  delirium  comes  on,  or  the  patient  lies  in  a  state 
of  partial  coma, — both  cough  and  expectoration  cease,  and 
the  patient  dies  of  apncea. 

You  will  find  these  symptoms  varying  somewhat  with  the 
age  and  peculiarities  of  the  individual  affected,  and  with 
the  diseases  which  it  may  complicate.  In  aged  persons,  or 
in  those  who  are  constitutionally  weak  from  any  cause,  the 
fever  is  very  apt  to  take  on  an  adynamic  type.  When  it 
occurs  in  connection  with  acute  blood  diseases,  it  is  likely 
to  come  on  very  insidiously,  without  any  of  the  usual  symp- 
toms of  the  disease  being  prominent. 


48  ACUTE   CAPILLARY   BRONCHITIS. 

PHYSICAL  SIGNS. — In  addition  to  the  signs  belonging  to 
simple  bronchitis,  the  percussion  sound  in  the  early  part 
of  the  disease  may  be  somewhat  exaggerated  in  the  infra- 
clavicular  regions,  on  account  of  the  dilated  condition  of  the 
air-cells  ;  as  the  disease  advances,  the  percussion  resonance 
may  be  diminished  on  account  of  pulmonary  oedema,  and 
the  accumulation  of  morbid  products  in  the  air-cells  and 
small  bronchi. 

Auscultation. — If  the  bronchitis  is  extensive,  the  vesicu- 
lar murmur  is  feeble  or  suppressed,  the  inspiration  may  be 
marked  by  high-pitched,  hissing  sibilant  rales  ; — as  the  dis- 
ease advances  the  subcrepitant  or  distinctive  rale  of  capil- 
lary bronchitis  is  heard  all  over  the  chest,  but  especially  in 
the  infra- scapular  region. 

If  the  subcrepitant  rales  are  abundant  and  are  heard  over 
the  whole  chest,  they  indicate  very  positively  the  existence 
of  general  capillary  bronchitis.  These  rales  may  be  present 
over  a  circumscribed  space  posteriorly,  as  the  result  of  the 
gravitation  of  the  fluid  secretion  from  the  larger  to  the 
smaller  tubes.  If  they  are  confined  to  the  apex  or  base  of 
one  lung,  with  resonance,  they  indicate  the  existence  of  a 
localized  capillary  bronchitis. 

DIFFERENTIAL  DIAGNOSIS. — From  the  rational  and  physi- 
cal signs  combined,  you  will  readily  make  the  diagnosis  of 
bronchitis  of  the  larger  tubes, — but,  capillary  bronchitis 
may  be  confounded  with  pneumonia,  pulmonary  oedema, 
and  with  acute  and  chronic  phthisis.  It  differs  from  simple 
bronchitis  in  the  great  frequency  of  the  respiration,  the 
extreme  dyspnoea,  the  interference  of  the  general  capillary 
circulation,  and  the  presence  of  the  hissing  sibilant  and  sub- 
crepitant rales.  It  is  distinguished  from  pneumonia  by  the 
absence  of  pain  in  the  side,  and  the  characteristic  pneumo- 
nic sputa ;  by  the  greater  frequency  and  labor  of  the  respira- 
tion, and  the  more  intense  dyspnoea ;  by  the  normal  or  ex- 
aggerated resonance  on  percussion,  by  the  presence  of  the 
subcrepitant  rales  on  both  sides  of  the  chest,  and  by  the 
absence  of  bronchial  respiration. 

I  shall  consider  the  points  of  differential  diagnosis  between 
capillary  bronchitis  and  phthisis  under  the  head  of  phthisis. 


TREATMENT.  49 

The  existence  of  the  physical  signs  of  capillary  bronchitis 
at  the  apex  of  one  lung,  accompanied  by  evidences  of  pul- 
monary consolidation  at  that  point,  always  leads  to  the  sus- 
picion of  incipient  phthisis. 

PROGNOSIS. — General  capillary  bronchitis  is  a  disease  at- 
tended with  great  danger.  Especially  is  this  the  case  when 
it  occurs  in  infancy  or  old  age,  or  when  it  supervenes  some 
grave  organic  disease,  as  phthisis,  Bright' s  disease,  heart 
disease,  and  acute  blood  diseases.  When  it  occurs  in  per- 
sons suffering  from  pulmonary  emphysema,  although  for  a 
time  the  symptoms  are  urgent,  it  rarely  proves  fatal. 

Among  the  unfavorable  symptoms  may  be  named  great 
difficulty  of  expectoration,  signs  of  accumulation  in  the 
bronchial  tubes,  shallow  breathing,  cessation  of  cough, 
urgent  dyspnoea,  with  evidences  of  apnoea  and  the  presence 
of  adynamic  symptoms. 

In  this  disease,  death  results  from  apnoea  caused  by  im- 
perfect oxygenation  of  the  blood. 

TREATMENT. — All  the  so-called  antiphlogistic  remedies 
lessen  if  they  do  not  destroy  the  chances  of  recovery.  From 
the  commencement  of  the  attack,  the  treatment  must  be 
supporting. 

In  general  capillary  bronchitis,  the  patient  must  be  kept 
in  bed,  the  surface  of  the  body  covered  with  flannel,  the 
temperature  of  the  apartment  must  range  from  68°  to  70°, 
and  the  air  must  be  moistened  with  steam.  Children  should 
be  placed  in  the  steam  tent,  as  advised  in  the  treatment  of 
membranous  croup.  Dry  cups  should  be  applied  over  the 
whole  surface  of  the  chest,  after  which  it  should  be  covered 
with  an  oil-silk  jacket. 

The  inhalation  of  steam  usually  increases  the  secretion 
from  the  bronchial  mucous  membrane,  facilitates  expectora- 
tion, and  for  a  time  at  least  relieves  the  difficult  breathing. 
If  symptoms  of  imperfect  oxygenation  are  developed,  the 
inhalation  of  oxygen  gas  in  connection  with  the  steam  will 
often  afford  the  most  marked  relief. 

The  internal  administration  of  muriate  of  ammonia  and 
chloride  of  potassium  in  five-  or  ten-grain  doses  every  two 
hours  to  the  adult  (two  grains  may  be  given  to  a  child  two 
4 


50  ACUTE   CAPILLARY  BRONCHITIS. 

years  of  age),  often  seems  to  have  a  controlling  influence 
over  the  inflammatory  processes.  The  so-called  expecto- 
rants are  of  little  service.  Sometimes  when  suffocation  is 
imminent  and  the  power  of  expectoration  is  entirely  lost, 
stimulating  emetics  will  be  found  of  service,  especially  in 
the  case  of  young  children  ;  the  action  of  the  emetic  seems 
to  supply  the  want  of  voluntary  power  to  expectorate,  and  it 
dislodges  the  accumulated  secretion  in  the  bronchial  tubes ; 
care  must  be  taken  not  to  repeat  them  so  often  as  to  produce 
exhaustion.  In  the  advanced  stage  of  the  disease,  when 
the  pulse  becomes  small  and  thready,  our  main  and  almost 
only  reliance  is  to  be  placed  on  the  free  administration  of 
quinine  and  brandy. 

You  must  bear  in  mind  that  the  main  object  of  treatment 
in  this  disease  is  to  sustain  the  life  of  your  patient  until 
the  inflammatory  process  has  passed  through  its  different 
stages.  As  regards  the  use  of  stimulants,  there  is  perhaps 
no  disease,  especially  of  childhood,  in  which  the  judicious 
administration  of  stimulants  is  so  markedly  beneficial. 
They  should  be  commenced  early  and  given  in  sufficiently 
large  quantities  to  overcome  the  signs  of  exhaustion,  which 
are  present  very  early  in  the  disease.  To  allay  spasm  of 
the  bronchial  tubes,  which  is  occasionally  present  in  this 
form  of  bronchitis  and  gives  rise  to  the  most  distressing 
paroxysms  of  dyspnoea,  full  doses  of  hydrocyanic  acid  are 
often  followed  by  most  marked  relief.  Opium  should  never 
be  given  in  general  capillary  bronchitis,  for  by  its  action  the 
power  of  expectoration  is  always  diminished,  and  it  favors 
the  dangerous  accumulation  of  inflammatory  products  in 
the  already  paralyzed  bronchial  tubes. 

You  should  always  study  each  case  by  itself,  investi- 
gating the  constitutional  conditions  under  which  it  occurs, 
and  so  modify  your  treatment  as  to  answer  the  indications. 
The  general  management  of  capillary  bronchitis,  associated 
with  Bright' s  disease,  would  be  very  different  from  that  of 
capillary  bronchitis  occurring  in  a  person  perfectly  healthy 
at  the  time  of  the  attack. 

During  the  whole  course  of  this  disease  the  patient  should 
receive  the  largest  amount  possible  of  concentrated  nutri- 


TREATMENT.  51 

tion, — the  yolk  of  eggs  and  milk  are  very  nutritive,  and  are 
generally  well  borne  by  this  class  of  patients.  Precaution 
must  be  taken  against  the  slightest  exposure  to  changes  in 
temperature  during  convalescence. 

Before  leaving  this  subject  I  will  make  mention  of  certain 
peculiarities  which  attend  the  catarrhal  bronchitis  of  young 
children.  It  differs  from  the  bronchitis  of  adults,  in  the 
greater  liability  of  the  extension  of  the  bronchial  inflamma- 
tion to  the  alveoli,  giving  rise  to  lobular  pneumonia  ;  also, 
in  the  liability  to  the  occurrence  of  atelectasis  or  collapse  of 
the  lobules,  the  result  of  the  plugging  up  of  the  small 
bronchi  from  accumulation  of  secretion  in  them.  The  occur- 
rence of  lobular  atelectasis  cannot  be  determined  with  cer- 
tainty either  by  the  rational  or  physical  signs.  It  may  be 
suspected  in  young  children,  whenever  the  physical  signs 
indicate  extensive  capillary  bronchitis,  accompanied  by  ex- 
treme dyspnoaa,  with  the  phenomena  of  non-oxygenization 
of  the  blood,  the  physical  signs  and  other  symptoms  of 
broncho-pneumonia  being  absent. 

The  development  of  lobular  pneumonia  is  certain  to  fol- 
low lobular  atelectasis,  if  the  life  of  the  patient  is  sufficiently 
prolonged  after  its  occurrence  ;  the  pneumonic  development 
is  marked  by  a  sudden  rise  in  temperature,  and  by  the 
characteristic  physical  signs  of  pulmonary  consolidation. 

In  the  treatment  of  the  bronchitis  of  young  children,  the 
liability  to  these  complications  should  always  be  borne  in 
mind. 


'"»"«" 


LECTURE   V. 


BRONCHITIS. 


Chronic  Catarrhal  Bronchitis. — Bronchial  Dilatation. — Croupous  Bronchitis. 

I  SHALL  invite  your  attention  this  morning  to  a  very  com- 
mon form  of  disease,  which  results  from  any  cause  which 
excites  and  keeps  up  a  low  grade  of  inflammation  of  the 
bronchial  mucous  membrane.  It  is  usually  a  disease  of 
adult  life.  One  of  its  chief  characteristics  is  its  tendency  to 
recurrence  ;  the  attacks  increase  in  severity  and  duration  at 
each  return,  until  the  person  is  rarely  free  from  it. 

Chronic  bronchitis  may  be  primary  or  secondary.  Pri- 
mary, when  it  is  the  result  of  wet  or  cold,  or  when  it  is 
excited  by  the  daily  inhalation  of  dust,  or  other  irritating 
substances.  Secondary,  when  due  to  some  constitutional 
vice,  as  gout,  rheumatism,  syphilis,  etc. ;  or  some  local 
affection,  as  cardiac  or  renal  disease. 

It  may  occur  as  a  complication  with  other  pulmonary 
affections,  as  phthisis,  pulmonary  emphysema,  etc. 

MORBID  ANATOMY. — As  in  acute  bronchitis,  any  portion 
of  the  bronchial  and  trachea!  membrane  may  be  the  seat  of 
the  inflammatory  action.  Thus  it  may  be  limited  to  the 
large  branches  of  the  bronchial  tree,  or  it  may  extend  into 
the  capillary  tubes.  Usually,  the  inflamed  membrane  has  a 
gray  or  reddish-blue  color.  In  the  more  chronic  cases,  its 
tissue  is  frequently  hypertrophied,  its  glands  are  enlarged 
and  prominent,  and  their  ducts  so  increased  in  size  that 
their  mouths  are  readily  visible.  As  a  rather  infrequent 
occurrence,  the  surface  of  the  membrane  presents  an  uneven 


MOKBID   AX  ATOMY.  53 

appearance,  due  to  the  presence  of  little  villosites  covered 
by  normal  epithelium ;  occasionally  follicular  ulcerations 
are  met  with.  These  villosites  and  ulcerations  are  usually 
arranged  longitudinally.  In  the  early  stage,  the  other  coats 
of  the  bronchial  tubes  may  be  weak  or  yielding  ;  later,  an 
increased  production  of  connective  tissue  takes  place,  lead- 
ing to  thickening  and  induration. 

The  cartilages  are  sometimes  normal,  at  other  times  hyper- 
trophied,  and  at  times  calcified.  In  the  posterior  wall  of 
the  trachea  and  the  larger  bronchi,  a  widening  of  the  mus- 
cular fibres  and  a  relaxation  of  the  bronchial  wall  takes 
place,  with  a  protrusion  of  the  mucous  membrane  and  its 
glands  through  fissures  in  its  middle  coat.  These  diverticuli 
may  involve  a  large  or  small  extent  of  the  posterior  bron- 
chial wall. 

In  very  chronic  cases,  where  there  has  been  a  puriform 
secretion  for  a  long  time,  not  unfrequently  the  bronchial 
mucous  membrane  presents  slight,  or  no  apparent  alter- 
ation. 

The  results  of  chronic  bronchitis  are  dilatation  and  stenosis 
of  the  bronchial  tubes,  an  accumulation  of  secretion  in  a 
state  of  cheesy  degeneration,  obstructing  more  or  less  their 
calibre,  pulmonary  emphysema,  and  induration  of  lung-tis- 
sue adjacent  to  the  inflamed  bronchi. 

Ulcerations  of  the  bronchial  membrane  rarely  occur;  if  they 
are  present  they  are  of  slight  extent,  and  for  the  most  part 
are  found  in  the  bronchitis  which  accompanies  phthisis. 

In  tertiary  syphilis,  chronic  bronchitis  is  due  to  gummy 
tumors  of  the  mucous  membrane  of  the  trachea  and  primary 
bronchi,  or  to  a  fibrous  induration  which  leads  to  stenosis. 

Fetid  Bronchitis. — An  excessively  fetid  odor  of  the  breath, 
and  of  the  matter  expectorated  in  the  course  of  a  chronic 
bronchitis,  may  find  no  explanation  after  death,  except  a  de- 
composition of  the  bronchial  secretion.  This  decomposition 
usually  takes  place  in  bronchial  dilatations  ;  but  by  clinical 
observation  and  autopsy,  we  find  it  may  arise  independently 
of  aii}7^  bronchial  dilatation. 

This  decomposition  of  the  secretion  may  exert  no  special 
injurious  influence,  or  it  may  give  rise  to  gangrene  of  the 


54  CHRONIC    CATAKIUTAL   BRONCHITIS. 

bronchial  mucous  membrane,  and  thus  may  spread  to  the 
lungs,  causing  a  more  or  less  extensive  gangrene  of  the 
lungs.  I  shall  consider  more  fully  the  changes  that  take 
place  in  the  small  bronchi  in  that  form  of  bronchial  catarrh 
which  accompanies  phthisis,  under  the  head  of  phthisis. 

ETIOLOGY. — The  most  interesting  part  of  the  history  of 
chronic  catarrhal  bronchitis  is  connected  with  its  etiology. 
When  it  is  primary,  whether  it  is  or  is  not  preceded  by  the 
acute  form,  it  arises  almost  entirely  from  external  causes ; 
such  as  cold  or  wet,  the  inhalation  of  dust  or  unwholesome 
air,  etc.  It  is  unquestionably  the  exception,  when  chronic 
bronchitis  is  developed  from  exposure  to  what  are  termed 
the  ordinary  causes  of  taking  cold,  without  some  special 
predisposition,  such  as  long-continued  mechanical  irritation 
of  the  bronchial  membrane,  constitutional  tendency,  or 
some  previously  existing  organic  disease. 

Acute  bronchitis  may  frequently  be  the  result  of  some 
temporary  exposure,  but,  if  it  becomes  chronic,  there  will 
almost  invariably  be  found  to  exist  a  predisposing  cause. 

Bronchial  irritation  may  exist,  perhaps  for  years,  as  the 
result  of  some  mechanical  irritation  (as  in  the  case  of  stone- 
cutters, grain-heavers,  etc.),  and  not  particularly  inconveni- 
ence the  individual,  until  an  acute  catarrh  is  developed  from 
exposure ;  this  invariably  passes  into  a  chronic  bronchial 
catarrh,  which  sooner  or  later  leads  to  the  development  of 
broncho-pneumonia,  and  we  have  a  condition  called  knife- 
grinder'  s  or  stone-cutter  s  phthisis. 

The  constant  inhalation  of  bad  or  unwholesome  air,  as  in 
badly  ventilated  apartments,  crowded  assemblies,  theatres, 
etc.,  produces  similar  bronchial  hypercemia,  which  renders 
the  individual  liable  to  have  an  attack  of  acute  bronchitis 
pass  into  chronic. 

Secondary  chronic  bronchitis,  or  that  which  arises  from 
some  previously  existing  ailment  or  constitutional  dyscrasia, 
is  of  more  frequent  occurrence. 

An  hereditary  tendency  to  gout  frequently  manifests  it- 
self in  a  form  of  chronic  bronchitis.  You  will  often  meet  in 
the  same  individual  attacks  of  bronchitis  and  gout  alterna- 
ting. In  some  instances  the  gouty  diathesis  only  produces 


ETIOLOGY.  55 

a  strong  predisposition  to  bronchitis,  which  requires  for  its 
development  some  external  exciting  cause,  much  slighter 
than  would  produce  the  disease  in  health ;  in  other  instan- 
ces, there  is  for  a  long  time  a  slight  bronchial  catarrh, 
which  as  life  advances  merges  slowly  into  chronic  bronchitis. 
N"ot  unfrequently  chronic  bronchitis  occurs  in  connection 
with  psoriasis  and  eczema,  and  these  affections  alternate 
with  each  other ;  as  one  disappears  the  other  manifests  it- 
self ;  frequently  there  is  associated  with  these,  gouty  kidney. 
Under  such  circumstances  we  cannot  avoid  the  conclusion 
that  these  different  affections  are  manifestations  of  the  same 
constitutional  vice,  which  is  called  gouty  diathesis. 

Pulmonary  emphysema  is  produced  in  many  instances  by 
chronic  bronchitis  ;  sometimes,  however,  it  occurs  indepen- 
dently of  it,  and  then  it  is  a  strong  predisposing  cause  to 
its  development. 

Disease  of  the  left  side  of  the  heart  predisposes  to  bron- 
chitis, and  when  bronchitis  does  occur  under  such  circum- 
stances, its  course  is  protracted  and  its  danger  increased. 
The  permanent  incompetency  of  the  mitral  valves  allows  re- 
gurgitation  through  the  mitral  orifice  during  contraction  of 
the  left  ventricle,  thus  overdistending  the  left  auricle  and 
impeding  the  flow  of  blood  from  the  lungs,  which  tends  to 
keep  up  a  constant  state  of  pulmonary  congestion.  If  bron- 
chitis occurs  under  such  circumstances  it  is  subacute  in 
character  and  chronic  in  duration.  Mitral  stenosis  may  pro- 
duce the  same  results. 

Chronic  alcoholismus  is  often  a  cause  of  chronic  bronchitis. 

SYMPTOMS. — The  symptoms  of  this  form  of  bronchitis  vary 
with  the  constitutional  and  local  causes  under  which  it  is 
developed.  There  are,  however,  certain  prominent  character- 
istics common  to  all  varieties,  the  most  constant  of  which  is 
cough  and  expectoration.  The  peculiarity  of  the  cough,  the 
quantity  and  quality  of  the  matter  expectorated,  determine 
to  a  great  extent  the  character  and  severity  of  the  bron- 
chitis. 

In  some  cases  the  cough  is  slight,  the  expectoration  moder- 
ate in  quantity,  and  muco-purulent  in  character ;  this  occurs 
in  the  mildest  variety  of  chronic  bronchitis,  a  variety  which 


56  CHEOXIC   CATAERHAL  BEOXCHITIS. 

comes  on  in  the  winter,  and  disappears  or  is  mitigated  in 
summer.  After  a  time  it  becomes  permanent,  and  is  liable 
to  exacerbations  in  cold,  damp  weather.  It  is  the  simplest 
form  of  chronic  bronchial  catarrh. 

In  another  class  of  cases  the  cough  is  violent  and  more 
constant,  severest  in  the  morning,  —the  expectoration  is 
either  tenacious  and  scanty,  or  thin,  semi-transparent,  and 
abundant ;  it  is  sometimes  streaked  with  blood,  and  frequent- 
ly is  difficult  to  expectorate  ;  it  varies  in  color  from  an  ash- 
yellow  to  a  deep  green  ; — it  is  slightly  aerated,  and  not  un- 
frequently  sinks  in  water.  Its  odor  varies :  sometimes  it  is 
sweet  and  nauseous  ;  at  other  times  it  has  the  same  fetor 
as  gangrene  of  the  lungs. 

The  microscope  shows  it  to  be  composed  of  granular  mat- 
ter, broken-down  epithelial  and  pus  cells,  and  sometimes 
of  blood-globules.  Some  cases  of  this  form  of  bronchitis 
are  attended  by  loss  of  flesh,  fever,  and  night- sweats.  It  oc- 
curs most  frequently  in  strumous,  broken-down  subjects, 
especially  those  given  to  alcoholic  excess.  More  or  less  ex- 
tensive bronchial  dilatations  are  usually  present  in  this  vari- 
ety of  bronchitis.  Again,  there  is  a  class  of  cases  in  which 
the  cough  is  exceedingly  troublesome  and  paroxysmal  in 
character, — the  expectoration  is  scanty,  consisting  of  small, 
rounded,  semi-transparent  masses  of  tough  mucus.  This 
variety  is  met  with  almost  exclusively  in  connection  with  pul- 
monary emphysema,  gout,  and  irritant  inhalations,  and  has 
received  the  name  of  dry  catarrh.  There  is  also  a  variety  of 
chronic  bronchitis,  not  unfrequently  met  with  in  old  people, 
especially  in  connection  with  heart  disease,  in  which  the 
cough  is  paroxysmal,  and  often  violent,  and  the  paroxysms 
are  attended  by  a  peculiar  flux  from  the  bronchi.  The  expec- 
toration often  amounts  to  four  or  five  pints  in  twenty-four 
hours,  and  is  either  watery  and  transparent,  or  gelatinous 
and  ropy,  resembling  an  emulsion  of  white-of-eggs  and 
water.  The  patient  often  finds  great  relief  after  a  paroxysm 
of  coughing  and  expectoration. 

In  some  cases  this  variety  of  bronchitis  is  accompanied  by 
loss  of  flesh  and  strength  ;  it  has  received  the  name  bron- 
shorrhcea. 


SYMPTOMS.  57 

In  all  these  varieties  there  is  dyspnoea  and  labored  respi- 
ration,— the  respiration  is  much  more  accelerated  in  other 
chronic  pulmonary  affections  than  in  bronchitis,  but  it  is 
never  so  laborious.  The  pulse  in  a  purely  chronic  bronchitis 
does  not  exceed  the  normal  frequency,  and  on  this  account  it 
may  readily  be  distinguished  from  pneumonia  and  phthisis  ; 
besides,  in  chronic  bronchitis  the  temperature  is  rarely  much 
above  the  normal  standard,  excepting  in  those  cases  which 
are  accompanied  by  a  fetid  expectoration. 

A  little  uneasiness  or  soreness  is  often  felt  behind  the 
sternum,  which  is  increased  by  violent  coughing  ;  but  pain 
in  the  side  is  rarely  present. 

Individuals  with  any  form  of  chronic  bronchitis  are  unable 
to  sustain  prolonged  physical  exertion  without  great  exhaus- 
tion, and  they  are  markedly  affected  by  atmospheric  changes. 

PHYSICAL  SIGNS. — These  are  very  nearly  the  same  as  in 
acute  bronchitis. 

Inspection  shows  labored  respiration,  with  diminished  ex- 
pansion on  inspiration. 

Vocal  fremitus  varies  :  if  the  bronchial  walls  of  the  larger 
tubes  are  thickened,  it  is  exaggerated  ;  if  the  tubes  are  ob- 
structed, it  is  diminished  or  absent.  In  the  simple  forms  of 
chronic  bronchitis,  the  vocal  fremitus  is  normal. 

The  percussion  sound  rarely  differs  from  that  in  health ; 
if  the  accumulation  of  a  thick  secretion  gives  rise  to  obstruc- 
tion in  some  of  the  bronchi,  then  temporary  dulness  on  per- 
cussion is  the  result. 

On  auscultation,  the  vesicular  murmur  is  more  or  less 
deficient  over  the  whole  chest,  and  the  respiratory  sound  is 
coarse,  loud,  and  harsh,  with  prolonged  expiration. 

After  free  expectoration,  it  will  often  be  audible  at  points 
where  it  has  been  inaudible  a  moment  before  ;  it  is  accom- 
panied, and  sometimes  entirely  masked,  by  every  variety  of 
rales,  chiefly  sonorous  and  sibilant.  Large  and  small  mu- 
cous rales  are  present  in  those  cases  in  which  there  is  abun- 
dant liquid  secretion. 

These  rales  are  constantly  varying  in  size  and  character, 
at  times  they  may  be  altogether  absent ;  they  are  altered  in 
character  and  position  by  coughing  and  by  full  inspiration. 


58  CHRONIC   CATARRHAL   BRONCHITIS. 

Vocal  resonance  is  normal,  diminished,  or  slightly  exagger- 
ated. 

DIFFERENTIAL  DIAGNOSIS.  —  The  diagnosis  of  chronic 
bronchitis  is  rarely  attended  with  difficulty,  except  in  con- 
nection with  pulmonary  phthisis. 

It  may  be  distinguished  from  pleuritic  effusions,  not  only 
by  the  cough  and  expectoration  which  attend  it,  but  by  the 
continuance  of  vocal  fremitus,  and  the  existence  of  reso- 
nance on  percussion  ;  from  pneumonic  consolidation,  by  the 
absence  of  bronchial  breathing,  the  rusty  expectoration,  the 
accelerated  breathing,  and  the  high  pulse  and  temperature 
which  attend  pneumonic  inflammation. 

In  those  cases  of  chronic  bronchitis  in  which  the  general 
health  suffers,  emaciation  takes  place,  and  bronchial  dilata- 
tion occurs ;  the  bronchitis  sometimes  so  closely  simulates 
phthisis  in  its  rational  and  physical  signs,  that  the  differ- 
ential diagnosis  is  exceedingly  difficult ;  the  points  of  differ- 
ence I  shall  more  fully  consider  under  the  head  of  pulmo- 
nary phthisis. 

PROGNOSIS. — This  disease  rarely  if  ever  directly  destroys 
life ;  but  when  it  occurs  in  the  old  and  feeble,  it  is  always 
attended  with  danger,  on  account  of  the  frequent  occurrence 
of  acute  attacks  involving  the  small  bronchi.  Any  pulmo- 
nary affection  associated  with  chronic  bronchitis  renders 
the  condition  of  the  patient  more  serious,  on  account  of  the 
liability  to  bronchial  obstruction  from  the  accumulation  of 
the  secretion  in  the  bronchial  tubes. 

It  is  very  apt  to  lead  to  the  development  of  pulmonary  em- 
physema, pulmonary  collapse,  dilated  bronchi,  and  fibrous 
phthisis. 

It  is  rarely  recovered  from,  when  it  occurs  in  persons  past 
middle  life. 

TREATMENT. — The  one  important  fact  for  you  to  bear  in 
mind  in  the  treatment  of  this  affection  is,  that  it  rarely  oc- 
curs as  a  primary  disease,  but  is  due  to  some  constitu- 
tional vice  of  previously  existing  disease.  You  must  remove 
your  patient  from  every  possible  source  of  bronchial  irrita- 
tion, and  guard  against  exposure  to  changes  of  temperature  : 
flannel  should  be  worn  next  the  skin  :  and  if  a  suitable  cli- 


TREATMENT.  59 

mate  cannot  be  obtained,  the  patient  must  keep  in-doorg 
during  bad  weather,  in  well-ventilated  apartments,  the  tem- 
perature of  which  should  range  from  65°  F.  to  70°  F.  Night 
air  and  cold  winds  must  be  avoided.  The  climate  best 
adapted  to  all  forms  of  bronchitis  is  one  with  a  moderately 
warm,  dry  atmosphere,  protected  from  cold  winds,  and  of 
moderately  high  altitude.  In  cases  that  are  attended  by 
emaciation,  a  long  sea-voyage  often  is  of  the  greatest  bene- 
fit. The  diet  at  all  times  should  be  most  nutritious. 

As  regards  the  use  of  stimulants,  no  definite  statement 
can  be  made  ;  but,  as  a  rule,  moderate  stimulation  is  of 
service. 

In  no  disease  is  a  careful  study  of  each  individual  case 
more  required.  The  immediate  and  remote  cause  of  the 
affection  must,  if  possible,  be  determined.  If  the  bronchitis 
is  the  result  of  an  irritant  inhalation,  removal  from  exposure 
to  this  is  the  first  thing  called  for.  If  cardiac  disease  exist, 
which  keeps  up  the  bronchial  affection  by  inducing  hyper- 
semia  of  the  mucous  membrane,  the  treatment  should  be 
directed  to  the  cardiac  affection,  and,  if  possible,  the  heart' s 
action  regulated.  If  a  gouty  or  rheumatic  diathesis  exist, 
the  use  of  colchicum  and  alkalies  is  indicated.  When 
pulmonary  emphysema  is  associated  with,  or  is  the  appa- 
rent cause  of  the  bronchitis,  the  internal  administration  of 
iodide  of  potassium  will  be  followed  by  most  marked  relief. 
In  general  ansemia  accompanying  bronchitis,  preparations 
of  iron  are  indicated  ;  in  fact,  in  the  great  majority  of  cases 
of  chronic  bronchitis,  a  general  tonic  plan  of  treatment  is 
attended  by  the  most  marked  benefit.  Quinine,  mineral 
acids,  bitter  vegetable  infusions,  combined  with  iron,  often 
prove  of  great  service.  Bronchial  catarrh,  alternating  with 
chronic  skin  affection,  yields  most  readily  to  preparations  of 
arsenic  and  sulphate  of  zinc. 

The  treatment  of  the  immediate  symptoms  must  depend 
upon  the  quantity  of  the  expectoration  ;  the  degree  of  diffi- 
culty which  attends  its  discharge,  and  the  presence  or  ab- 
sence of  any  spasmodic  action  of  the  bronchial  tubes. 
When  the  bronchial  secretions  are  excessive  in  quantity, 
steam  inhalations  of  tar,  creosote,  and  naphtha  are  often  of 


60  CHRONIC   CATARRIIAL   BRONCHITIS. 

great  service  in  limiting  their  formation ;  the  vapor  of 
iodine,  muriate  of  ammonia,  and  the  different  balsams  are 
also  of  service  for  accomplishing  the  same  purpose. 

These  remedies  may  be  demanded  internally  at  the  same 
time.  When  the  power  of  expectoration  is  deficient,  owing 
to  the  adhesive  character  of  the  expectoration,  stimulating 
expectorants  are  indicated,  such  as  senega,  serpentaria, 
camphor,  tincture  of  benzoin,  combined  with  alkalies,  as 
carbonate  of  potash,  soda,  etc. 

In  those  cases  where  the  bronchial  membrane  is  extremely 
irritable,  and  the  secretion  scanty,  and  the  cough  is  attend- 
ed by  violent  paroxysms,  narcotics  and  sedatives  should  be 
administered  in  full  doses  ;  opium,  hydrocyanic  acid,  hyos- 
cyamus,  belladonna,  and  conium  are  the  most  reliable  agents 
of  this  class. 

When  there  is  much  spasm  of  the  bronchi,  shown  by  the 
breathing  and  cough,  a  few  drops  of  ether  or  chloroform 
may  be  inhaled  ;  when  the  tendency  to  the  spasm  is  great, 
the  narcotics  and  sedatives  already  referred  to  should  be 
administered.  Tincture  of  cannabis  indica  acts  well  in 
some  of  these  cases. 

In  all  varieties  of  chronic  bronchitis,  localized  counter- 
irritation  over  the  seat  of  the  most  extensive  bronchial 
changes  may  sometimes  be  employed  with  benefit ;  such 
as  may  be  produced  by  dry  cups,  sinapisms,  blisters,  cro- 
ton-oil,  turpentine,  etc. 

It  is  never  necessary  or  desirable  to  abstract  blood,  either 
locally  or  generally. 

Occasionally  emetics  may  be  employed  with  benefit  when 
the  bronchial  secretion  accumulates  in  the  larger  tubes  and 
cannot  be  expectorated. 

Before  leaving  the  subject  of  chronic  bronchitis,  there  are 
some  points  in  connection  with  dilatation  of  the  bronchi, 
concerning  which  I  wish  to  say  a  few  words.  Under  the 
head  of  Morbid  Anatomy  of  Bronchitis,  I  stated  that  the 
inflammatory  changes  wThich  take  place  in  the  bronchial 
walls  cause  dilatations  of  the  bronchi ;  these  dilatations 
may  be  cylindrical,  fusiform,  or  sacculated.  In  those 
bronchial  dilatations  which  occur  as  the  result  of  chronic 


MOEBID   ANATOMY.  61 

bronchitis,  the  walls  of  the  dilated  bronchi  are  hyper- 
trophied,  the  mucous  membrane  is  thickened  and  may  be 
covered  over  with  little  papillary  outgrowths.  The  sub- 
mucous  tissue  and  mucous  glands  are  more  or  less  hyper- 
trophied.  In  children,  not  unfrequently  the  bronchial  dila- 
tation caused  by  bronchitis  disappears  as  the  bronchitis 
subsides.  The  lung-tissue  in  close  proximity  to  the  bron- 
chial dilatation  will  be  found  altered  in  various  ways ;  it 
may  be  in  a  state  of  fibrous  induration,  emphysematous, 
or  the  seat  of  lobular  pneumonia. 

In  addition  to  the  bronchial  dilatation  which  occurs  as 
the  result  of  degeneration  of  the  bronchial  walls  in  the  dif- 
ferent stages  of  bronchitis,  atelectasis,  fibrous  induration, 
and  other  structural  changes  in  lung-tissue,  as  well  as  old 
pleuritic  thickenings,  may  be  the  cause  of  bronchial  dilata- 
tion. These  bronchial  changes  I  shall  consider  more  fully 
in  connection  with  the  history  of  pulmonary  phthisis. 

In  all  forms  of  bronchial  dilatation  the  small  bronchi  are 
more  frequently  involved  than  the  larger  ;  the  situation  of 
these  dilatations  are  determined  by  the  condition  of  the 
lungs  prior  to  their  development,  although  the  bronchi  of 
the  lower  lobes  are  most  frequently  affected. 

The  most  characteristic  symptoms  that  attend  these  dila- 
tations are  the  changes  in  the  breath  and  sputa,  to  which  I 
have  already  referred  under  the  head  of  fetid  bronchitis. 
Their  farther  history  I  shall  postpone  until  I  reach  the  sub- 
ject of  pulmonary  phthisis. 

Narrowing  or  stenosis  of  the  bronchi  very  often  attends 
or  causes  bronchial  dilatation.  It  may  also  be  produced  by 
pressure  of  tumors  situated  external  to  the  bronchi,  as 
aneurism,  enlarged  glands,  etc. ;  or  from  contraction  of  the 
bronchial  walls,  which  results  from  the  development  of 
cicatricial  tissue  in  connection  with  ulceration  of  a  syphi- 
litic or  inflammatory  origin.  These  also  are  more  or  less  con- 
nected with  the  history  of  the  anatomical  changes  of  pulmo- 
nary phthisis,  and  will  be  best  considered  in  that  connection. 

CROUPOUS  BRONCHITIS. 

Under  this  head  I  shall  consider  croupous  or  plastic  in- 


62  PLASTIC   BRONCHITIS. 

flammation  of  the  bronchial  mucous  membrane,  as  it  occurs 
independently  of  laryngeal  croup  on  the  one  hand,  or  of 
croupous  pneumonia  on  the  other,  or  of  that  form  of 
catarrhal  bronchitis  during  the  course  of  which  a  few  mem- 
branous flakes  are  expectorated.  This  disease  may  pursue 
either  an  acute  or  chronic  course.  Both  forms  are  rare ; 
the  acute  is  the  most  infrequent. 

MOIIBID  AJSTATOMY. — It  differs  from  catarrhal  bronchitis 
in  the  character  of  the  exudation,  as  plastic  material  is 
poured  out  into  the  tubes  in  the  form  of  casts,  which  are 
either  solid  or  hollow,  according  as  the  large  or  small  tubes 
are  affected. 

In  the  chronic  form,  the  membranous  exudation  occurs 
only  over  a  circumscribed  portion  of  the  bronchial  mem- 
brane ;  in  the  acute,  it  is  distributed  over  a  greater  portion 
of  the  bronchi.  The  membrane  may  be  firmly  adherent  or 
loosely  attached  to  the  mucous  surface.  These  casts  are  of 
a  whitish  color,  sometimes  dotted  over  with  blood-spots. 
Microscopically,  they  consist  of  fibrillated  fibrine,  abundant 
granular  matter,  exudation  corpuscles,  and  fusiform  ovoid 
cells. 

In  some  cases  no  membrane  exists ;  the  bronchial  mem- 
brane is  pale  and  congested.  The  epithelium  in  all  cases 
is  retained. 

ETIOLOGY. — There  is  no  known  special  exciting  or  pre- 
disposing cause  to  this  disease — it  is  supposed  to  be  due  to 
some  diathetic  state.  It  is  most  frequently  met  with  in 
young  adults,  and  occurs  more  frequently  in  females  than 
in  males,  and  in  those  of  feeble,  delicate  constitutions, 
rather  than  in  those  who  are  strong  and  healthy. 

SYMPTOMS.  —  The  acute  form  is  usually  preceded  by 
catarrhal  symptoms  of  short  duration.  It  is  attended  by 
fever,  by  dyspnoea  (often  severe),  by  a  dry,  hoarse,  ringing 
cough  (not  as  stridulous  as  in  croup),  and  by  a  sense  of 
constriction  and  oppression  across  the  chest.  After  severe 
paroxysms  of  coughing,  either  fragments  of  membrane,  or 
membranous  casts  or  cylinders  are  expectorated.  The 
membranous  expectoration  in  rare  instances  is  wanting, 
and  occasionally  not  even  cough  is  present.  There  are  no 


SYMPTOMS.  63 

symptoms  of  laryngeal  obstruction.  When  the  disease 
progresses  towards  a  fatal  termination,  the  dyspnoea  rapid- 
ly increases  in  severity,  and  is  finally  superseded  by  those 
phenomena  which  precede  death  by  asphyxia. 

The  chronic  form  is  generally  preceded  by  catarrhal 
bronchitis,  which  sometimes  has  lasted  for  a  long  time  ; 
severe  haemoptysis  may  have  preceded  its  development. 

Not  unfrequently,  in  pulmonary  phthisis,  where  haemop- 
tysis has  occurred,  casts  of  the  bronchial  tubes  are  expec- 
torated, which  are  nothing  more  than  decolorized  blood- 
clots. 

The  history  of  the  chronic  form  of  plastic  bronchitis  is 
rarely  a  continuous  one,  but  is  made  up  of  intervals  of 
health  and  paroxysms  of  disease  ;  during  the  latter,  expec- 
toration of  membrane  in  fragments  or  casts  occurs.  Their 
removal  is  often  preceded  by  fits  of  severe  coughing,  and 
by  paroxysms  of  dyspnoea  of  variable  intensity,  lasting 
usually  a  few  hours,  sometimes  a  day  or  more  ;  at  other 
times  simple  sneezing  effects  their  removal. 

Generally,  along  with  the  membrane,  there  is  catarrhal 
expectoration,  in  which  small  portions  of  membrane  may 
be  hidden.  In  about  one-third  of  the  cases,  haemoptysis 
(generally  slight)  has  either  preceded  or  accompanied  the 
membranous  expectoration.  The  membranous  exudation, 
if  it  comes  from  the  large  bronchi,  is  in  the  form  of  casts  ;  if 
from  the  small,  it  is  in  the  form  of  cylinders.  Occasion- 
ally, there  is  mucus  or  blood  in  the  interior  of  the  casts, 
while  often  streaks  of  blood  are  present  on  their  exterior. 
The  casts  are  of  variable  thickness  and  length, — usually 
two  or  three  inches  long,  laminated,  and  of  a  whitish  or 
grayish  color.  Microscopically,  they  are  composed  of  a 
structureless  mass,  more  or  less  fibrous  in  character,  in 
which  cells  are  embedded,  more  particularly  pus-cells. 

During  the  interval  between  the  paroxysms  in  uncompli- 
cated plastic  bronchitis,  the  general  health  is  good,  and 
fever  is  not  present. 

PHYSICAL  SIGNS. — These  depend  upon  the  obstruction 
produced  by  the  membrane,  sometimes  upon  the  vibration 
of  a  portion  of  it,  and  on  coincident  catarrh. 


64  PLASTIC   BRONCHITIS. 

When  the  bronchial  tubes  are  obstructed,  there  is  feeble- 
ness or  absence  of  the  respiratory  murmur  ;  in  the  chronic 
form,  over  a  limited  portion  of  the  chest ;  in  the  acute,  over 
a  large  extent.  At  the  same  time,  the  percussion  note  may 
be  normal,  extra-resonant,  or  dull  ;  the  latter  existing  when 
collapse  of  the  lung  has  taken  place,  disappearing,  it  may 
be,  immediately  after  membranous  expectoration,  while  the 
respiratory  murmur  regains  its  normal  character,  thus 
masking  the  exact  seat  of  the  disease.  Flapping  and  rub- 
bing sounds  have  been  described  as  a  result  of  the  vibration 
of  the  membrane.  Dry  and  moist  rales  are  also  usually 
present,  due  either  to  the  narrowing  of  the  tubes,  or  to 
coincident  bronchial  catarrh. 

DIFFERENTIAL  DIAGNOSIS. — This  form  of  bronchitis  may 
be  mistaken  for  acute  catarrhal  bronchitis,  pneumonia,  or 
pleurisy. 

The  history  of  the  case,  the  character  of  the  paroxysm, 
the  membranous  expectoration,  and  the  accompanying  phy- 
sical signs,  will  generally  enable  you  to  make  the  diagnosis 
of  plastic  bronchitis  ;  without  the  membranous  expectora- 
tion, however,  the  differential  diagnosis  between  acute 
croupous  and  acute  catarrhal  bronchitis  cannot  be  made. 
The  absence  of  the  symptoms  which  usually  attend  pneu- 
monia and  pleurisy  serves  to  exclude  them  from  the  ques- 
tion of  diagnosis. 

PROGNOSIS. — With  the  acute  form,  more  than  one-half 
die ;  with  the  chronic  form,  if  death  occurs,  it  is  due  to 
some  complication,  so  that  in  uncomplicated  cases  of  chronic 
plastic  bronchitis,  the  prognosis  as  regards  life  is  good ; 
but,  the  disease  having  once  occurred,  it  is  very  apt  to 
return. 

The  duration  of  the  disease  varies.  In  the  fatal  cases, 
when  the  disease  is  acute,  it  lasts  from  three  to  ten  days ; 
in  those  cases  that  recover,  it  lasts  from  ten  to  fourteen 
days.  In  the  chronic  form,  the  paroxysms  usually  last  ten 
or  twelve  days,  and  recur  at  longer  or  shorter  intervals  for 
months  or  years.  Complete  recovery  is  rare.  Croupous 
bronchitis  is  very  likely  to  lead  to  pneumonia  and  pulmo- 
nary phthisis. 


TREATMENT.  65 

TREATMENT. — The  acute  form  is  to  be  treated  the  same 
as  croupous  laryngitis.  In  the  chronic  form,  during  the 
paroxysm,  alkaline  steam  inhalations  should  be  resorted 
to,  with  the  hope  of  removing  the  membrane  as  quickly  as 
possible,  and  the  patient  should  be  kept  in  a  warm,  equable 
temperature.  During  the  interval,  the  general  system 
should  be  invigorated  in  every  possible  way,  and  all  ex- 
posure to  the  causes  of  bronchial  irritation  should  be  avoid- 
ed. The  internal  administration  of  iodide  of  potassium  has 
been  highly  recommended  ;  quinine,  iron,  and  cod-liver  oil 
are  often  called  for.  If  the  recurrence  of  the  paroxysm 
continues,  a  change  to  a  warm  climate  or  a  long  sea-voyage 
must  be  tried.  There  is  no  known  remedy  or  plan  of  treat- 
ment which  promises  a  cure  in  this  disease. 

5 


LECTURE  VI. 


ASTHMA. 

Spasmodic  Asthma. — Hay- Asthma. — Whooping-cough. 

1  WILL  this  morning  continue  the  history  of  diseases 
of  the  bronchi  by  inviting  your  attention  to  spasmodic 
asthma.  Concerning  few  diseases  has  there  been  such 
diversity  of  opinion  in  regard  to  their  exact  nature  as  con- 
cerning asthma. 

MORBID  ANATOMY. — With  our  present  knowledge  of  this 
affection  we  are  compelled  to  regard  it  as  simply  a  spasmo- 
dic affection  of  the  bronchi,  which  gives  rise  to  a  dyspnoaa 
of  a  paroxysmal  character.  The  spasmodic  contractions 
of  the  bronchial  tubes,  which  develop  the  phenomena  of  the 
paroxysms,  are  due  to  reflex  nervous  action  ;  in  this  respect 
it  may  be  regarded  as  a  neurosis,  which  depends  upon  tlie 
existence  of  a  peculiar  diathesis. 

Although  the  paroxysms  are  usually  accompanied  by  all 
the  symptoms  of  catarrh,  and  sometimes  of  a  severe  catarrh, 
still  not  unfrequently  the  catarrhal  symptoms  are  altogether 
wanting.  The  catarrh,  when  present,  may  precede  the  par- 
oxysm, or  it  may  not  come  on  until  its  close.  Although 
bronchitis  often  plays  an  important  part  in  the  development 
of  asthma,  it  only  acts  as  an  exciting  cause,  as  there  must 
exist  a  special  condition  of  the  system  without  which  the 
paroxysm  could  not  have  been  produced. 

The  asthmatic  attacks  may  occur  in  persons  suffering 
from  organic  diseases  of  the  heart  or  lungs,  but  all  true 
asthma  is  spasmodic. 


ETIOLOGY.  67 

ETIOLOGY. — Unquestionably,  the  primary  cause  of  asth- 
ma is  some  constitutional  idiosyncrasy  which  is  generally 
hereditary.  It  is  a  diathetic  disease,  and  like  all  such  dis- 
eases may  be  directly  transmitted  from  parent  to  offspring. 
It  is  believed  by  some  to  be  connected  with  a  gouty  or 
rheumatic  diathesis.  No  period  of  life  is  exempt  from  this 
disease  ;  I  have  seen  a  well-marked  paroxysm  of  asthma  in 
an  infant  six  weeks  old,  born  of  an  asthmatic  mother. 

The  exciting  causes  of  the  asthmatic  paroxysms  may  be 
grouped  into  three  classes  : 

First. — Those  cases  in  which  the  bronchial  spasm  is  pro- 
duced by  some  material  respired  which  acts  directly  on 
the  bronchial  mucous  membrane.  In  this  class  are  included 
all  those  cases  of  asthma  in  which  the  asthmatic  parox- 
ysms are  excited  by  irritating  inhalations,  such  as  ipecac- 
uanha powder,  smoke,  emanations  from  newly-mown  hay, 
certain  atmospheric  conditions,  and  the  emanations  from 
certain  animals. 

Second. — Those  cases  which  are  reflex  in  their  origin.  In 
this  class  are  included  those  in  which  the  asthmatic  parox- 
ysms follow  errors  in  diet,  an  overloaded  rectum,  uterine 
irritation,  the  sudden  application  of  cold  to  the  surface, 
violent  mental  emotions,  and  those  that  are  of  periodic 
origin. 

Third. — Those  cases  which  occur  as  complications,  or  in 
connection  with  bronchitis,  heart-disease,  or  emphysema, 
and  are  most  likely  to  occur  after  fatigue  and  physical 
exertion.  Each  individual  subject  to  asthma  is  susceptible 
only  to  his  own  peculiar  exciting  cause. 

That  form  of  asthma  termed  hay-asthma,  which  is  pro- 
duced by  emanations  from  newly-mown  hay  or  other  vege- 
table emanations,  is  always  preceded  or  accompanied  by 
coryza  and  bronchitis  ;  persons  may  have  the  coryza  and 
bronchitis  for  years  without  having  the  asthmatic  parox- 
ysm, yet  the  paroxysms  are  certain  to  come  sooner  or  later, 
and  differ  in  no  respect  from  other  asthmatic  paroxysms. 

SYMPTOMS. — An  attack  of  asthma  may  or  may  not  be 
preceded  by  precursory  symptoms  ;  the  majority  of  persons 
suffering  from  this  disease  know  when  the  attack  is  coming 


68  SPASMODIC   ASTHMA. 

on,  by  certain  sensations  which  they  alone  can  appreciate, 
and  which  greatly  vary  in  different  individuals,  such  as  ex- 
treme drowsiness  or  wakefulness,  headache,  itching  of  the 
chin,  etc. 

Ordinarily,  the  individual  goes  to  bed  as  well  as  usual 
and  quietly  falls  asleep  ;  after  an  hour  or  two,  while  he  is 
still  asleep,  the  characteristic  wheezing  commences,  and  soon 
he  is  awakened  by  a  most  distressing  attack  of  dyspnoaa. 
He  feels  as  if  his  chest  were  compressed,  sits  up  in  bed  and 
rests  his  elbows  on  his  knees,  and  with  fixed  head,  elevated 
shoulders  and  mouth  open,  labors  for  breath.  His  face  be- 
comes red  and  turgid  or  livid,  his  eyes  prominent,  his  sur- 
face covered  with  perspiration ;  he  springs  out  of  bed  and 
hastens  to  an  open  window  in  search  of  air ;  respiration  is 
noisy  and  wheezing,  his  inspirations  are  short  and  jerking, 
while  the  expirations  are  prolonged  and  terminate  with  a 
sudden  effort  at  expulsion.  If  the  bronchial  spasm  is  pro- 
longed, the  surface  temperature  falls  below  the  normal 
standard,  the  extremities  are  cold,  blue,  and  shrunken,  and 
the  patient  appears  to  be  dying.  The  pulse  during  the 
paroxysm  is  small  and  feeble  in  proportion  to  the  intensity 
of  the  dyspnoea.  The  duration  of  the  paroxysm  varies  ;  at 
one  time  it  lasts  only  a  few  minutes,  at  another  time  an 
hour  or  two,  in  rare  instances  it  may  continue  two  or  three 
days  without  intermission.  As  the  paroxysm  passes  off, 
the  patient  begins  to  cough  and  expectorate ;  in  some 
patients,  the  expectoration  consists  of  a  few  small,  rounded 
masses  of  mucus,  in  others  it  is  profuse  and  watery.  The 
paroxysm  recurs  after  intervals  of  varying  length  ;  gome  ex- 
perience an  attack  only  annually,  others  monthly,  and  others 
only  when  subjected  to  their  own  peculiar  exciting  cause. 

During  the  interval,  if  the  asthma  is  not  due  to  any  or- 
ganic disease,  the  condition  of  those  subject  to  the  asthma 
varies ;  some  are  perfectly  well,  others  constantly  have  a 
sense  of  thoracic  constriction  which  renders  the  breathing 
somewhat  labored,  especially  during  active  exercise.  Some 
suffer  severely  from  a  bronchial  or  nasal  catarrh.  When 
the  catarrhal  element  predominates,  the  asthmatic  parox- 
rsms  are  excited  by  slight  exposure. 


PHYSICAL    SIGNS.  69 

Immediately  after  a  paroxysm,  usually  there  is  a  feeling 
of  exhaustion  which  passes  off  in  a  few  hours,  and  the 
patient  experiences  a  marked  sense  of  relief,  and  has  for 
a  time  an  almost  certain  immunity  from  a  repetition  of  the 
attack. 

PHYSICAL  SIGNS. — During  the  paroxysm  inspection  shows 
labored  respiration,  while  the  upper  part  of  the  chest  is 
almost  motionless,  and  the  muscles  of  the  neck  rigid ;  the 
inferior  costal  and  abdominal  respiration  is  labored,  the 
act  of  inspiration  is  slower  than  in  health,  and  expiration  is 
more  active  and  violent. 

Vocal  fremitus  and  vocal  resonance  are  normal. 

The  percussion  sound  is  slightly  exaggerated. 

On  auscultation,  the  respiratory  murmur  is  jerking  and 
irregular  ;  sometimes  it  is  exaggerated,  at  other  times  it  is 
suppressed.  Sibilant  and  sonorous  rales  of  a  high-pitched, 
hissing,  and  wheezing  character  are  diffused  over  the  whole 
chest,  often  loud  enough  to  be  heard  at  a  distance  from  the 
patient.  These  rales  are  constantly  changing  their  char- 
acter and  site,  disappearing  at  one  point  and  making  their 
appearance  at  another.  At  the  close  of  the  paroxysm,  some 
moist  rales  may  be  heard. 

DIFFERENTIAL  DIAGNOSIS. — Spasmodic  asthma  will  rarely 
be  confounded  with  any  other  disease,  if  its  rational  and 
physical  signs  are  properly  appreciated.  The  phenomena 
of  a  paroxysm  are  quite  distinctive,  while  the  physical 
signs  are  unmistakable.  The  only  affections  with  which 
there  is  a  possibility  of  its  being  confounded  are  spasmodic 
affections  of  the  larynx,  acute  capillary  bronchitis,  angina 
pectoris,  hydrothorax,  pulmonary  oedema,  and  congestion. 

It  is  easily  distinguished  from  laryngeal  affections,  from 
the  fact  that  there  is  no  change  in  the.  voice,  which  is  so 
characteristic  of  laryngeal  spasm.  It  is  distinguished  from 
bronchitis  by  the  slowness  of  the  respiration  and  the  ab- 
sence of  subcrepitant  rales, — from  angina  pectoris,  by  the 
presence  of  sibilant  and  sonorous  rales, — from  hydrothorax, 
by  the  fact  that  there  is  resonance  on  percussion  over  the 
entire  thorax. 

Asthmatic  dyspnoea  and  cardiac  dyspnoea  are  sometimes 


70  SPASMODIC   ASTHMA. 

confounded  ;  in  some  respects  they  resemble  each  other, — 
both  are  paroxysmal,  both  are  intense,  and  both  generally 
occur  at  night.  In  both,  the  respiration  may  be  perfectly 
normal  between  the  attacks,  but  a  careful  physical  exam- 
ination will  enable  you  to  determine  whether  the  dyspnoea 
is  asthmatic  or  cardiac. 

PROGNOSIS. — Death  rarely,  if  ever,  occurs  from  uncom- 
plicated asthma.  Asthmatic  patients  are  frequently  long- 
lived,  which  may  be  accounted  for  from  the  fact  that  they 
are  compelled  to  observe  the  most  rigid  hygiene  in  order  to 
avoid  their  asthmatic  attacks.  The  fact  that  a  person  has 
had  one  asthmatic  attack,  is  presumptive  evidence  that  he 
will  have  another.  The  prognosis  as  to  recovery  is  hopeful 
in  proportion  to  the  youth  of  the  patient.  If  the  attacks 
only  come  on  at  long  intervals,  and  are  not  severe  or  pro- 
longed ;  if,  during  the  intervals,  the  patient  is  well,  and 
there  is  no  organic  disease  ;  if  the  paroxysms  can  be  traced 
to  some  obvious  cause  which  may  be  avoided,  the  prognosis 
as  to  complete  recovery  is  good. 

TREATMENT. — In  regard  to  the  treatment  of  this  affection 
there  are  two  things  to  be  considered  :  how  we  may  relieve 
the  paroxysms  when  they  occur,  and  how  we  may  prevent 
their  occurrence.  I  shall  first  consider  the  treatment  of  the 
paroxysms. 

When  called  to  a  patient  in  an  asthmatic  paroxysm,  you 
must  first  ascertain  the  exciting  cause,  and  if  it  is  still  in 
operation,  if  possible  remove  it.  If  the  paroxysm  is  de- 
pending upon  an  overloaded  stomach,  at  once  an  emetic- 
should  be  administered  ;  if  upon  a  loaded  rectum,  an  enema 
should  be  given  ;  if  smoke,  dust,  or  any  animal  or  vegetable 
emanation  is  the  cause  of  the  attack,  this  cause  should  be 
removed.  If,  in  a  certain  locality,  the  attacks  of  asthma 
are  of  frequent  occurrence,  the  patient  should  remove  to 
one  where  he  is  free  from  asthmatic  paroxysms.  Not  un- 
frequently  the  removal  of  the  exciting  cause  will  be  all  that 
is  necessary  for  the  relief  of  the  patient. 

If  the  exciting  cause  cannot  be  removed,  or  if  its  removal 
is  not  followed  by  a  relief  of  the  paroxysm,  free  ventilation 
should  be  secured,  and  the  patient  should  be  placed  in  a 


TREATMENT.  71 

position  in  which  respiration  may  be  carried  on  with  as 
little  mechanical  impediment  as  possible ;  usually,  the  best 
position  during  an  attack  is  the  sitting  posture — in  a  chair 
which  will  give  support  to  the  arms,  and  so  elevate  the 
shoulders. 

Having  placed  your  patient  under  the  most  favorable  cir- 
cumstances for  the  relief  of  the  paroxysm,  the  next  thing  is 
to  select  those  remedial  agents  best  adapted  to  the  case.  This 
selection  will  be  very  much  influenced  by  the  patient' s  own 
experience.  The  great  majority  of  persons  suffering  from 
asthma  have  a  practical  knowledge  of  those  remedies  best 
suited  to  their  case.  Different  cases  are  relieved  by  very 
different  remedies.  These  different  remedies  may  be  divided 
into  three  classes — depressants,  sedatives,  and  stimulants. 
Among  the  leading  depressants  are  antimony,  ipecacuanha, 
tobacco,  and  lobelia.  If  a  patient  has  previously  been  re- 
lieved by  the  use  of  depressants,  it  is  well  to  inquire  which 
one  of  this  class  he  made  use  of.  The  manner  in  which 
relief  is  obtained  by  this  class  of  remedies  is  by  producing 
in  the  patient  a  condition  in  which  there  is  complete  relaxa- 
tion of  the  spasm.  Sometimes  this  may  be  accomplished 
by  the  administration  of  one  full  dose  of  ipecacuanha. 
Whichever  one  of  this  class  is  employed,  it  should  be  given 
until  its  decided  effects  are  produced. 

Sedatives  seem  to  act  in  two  ways  ;  some  act  locally  on 
the  nervous  system  of  the  lungs,  but  the  majority  give  re- 
lief'by  their  action  on  the  general  nervous  system. 

Those  which  experience  has  shown  to  be  of  the  most 
value  in  arresting  the  asthmatic  spasm  are — stramonium, 
chloroform,  ether,  opium,  cannabis  indica,  hyoscyamus, 
and  the  fumes  of  burning  nitre  paper. 

Certain  persons  will  be  promptly  relieved  by  the  inhala- 
tion of  the  fumes  of  stramonium  leaves, — others  by  the  in- 
halation of  chloroform.  Perhaps  there  is  no  agent  in  this 
class  that  will  so  speedily  and  completely  relieve  the  spasm 
as  chloroform  ;  but  the  relief  is  only  temporary  ;  so  soon  as 
its  stupefying  effects  have  passed  away,  the  paroxysm  gen- 
erally returns  with  increased  violence. 

In  this  class  of  remedial  agents,  that  which  I  have  used 


72  SPASMODIC  ASTHMA. 

most  successfully  is  opium  given  in  full  doses — small  doses 
are  unavailing.  One-half  a  grain  of  the  sulphate  of  mor- 
phia should  be  administered  at  once.  I  prefer  to  use  the 
remedy  hypodermically.  Atropine  may  be  combined  with 
the  morphia  ;  there  are  cases  which  are  quickly  relieved  by 
this  combination,  which  are  not  relieved  by  the  use  of  either 
of  these  drugs  alone. 

Mtre  paper  is  one  of  the  oldest  and  best  remedies  for 
asthma  (it  is  prepared  by  dipping  ordinary  paper  in  a  solu- 
tion of  saltpetre).  How  it  acts  is  not  well  understood ;  it 
certainly  does  not  act  by  relieving  the  bronchial  irritation, 
for,  as  a  rule,  the  patient  is  not  relieved  if  bronchitis  is 
associated  with  the  asthma.  When  this  remedy  is  em- 
ployed, it  is  necessary  that  the  apartment  occupied  by  the 
patient  be  filled  with  the  fumes  of  the  burning  paper.  If 
the  remedy  is  to  act  favorably,  it  will  do  so  quickly,  and 
its  administration  must  not  be  prolonged,  if  relief  is  not 
promptly  obtained. 

Among  stimulants,  the  two  principal  remedies  are  coffee 
and  alcohol.  Coffee  is  the  most  generally  efficacious.  It 
should  be  taken  strong,  without  milk  or  sugar,  and  as  hot 
as  it  can  be  swallowed  ;  it  should  always  be  taken  on  an 
empty  stomach.  Not  unfrequently  a  paroxysm  of  asthma 
can  be  warded  off  by  taking  two  or  three  cups  of  strong 
coffee  immediately  upon  the  accession  of  the  first  asthmatic 
symptom. 

Alcohol  is  another  stimulant  which  experience  has  led 
me  to  regard  very  highly  as  a  remedy  for  asthma.  It  is  of 
little  importance  what  alcoholic  stimulant  is  employed,  but 
it  must  be  taken  hot  and  strong,  and  in  sufficiently  large 
doses  for  the  patient  to  feel  its  intoxicating  effects.  As  a 
rule,  asthmatic  patients  will  bear  large  quantities  of  alco- 
holic stimulants  without  becoming  intoxicated. 

There  has  been  much  discussion  as  to  the  manner  in  which 
stimulants  act  in  this  disease. 

In  this  connection,  there  is  one  fact  worthy  of  notice, — 
asthmatic  patients  who  are  relieved  by  stimulants  have  their^ 
paroxysms  come  on  while  they  are  sleeping.  During  sleep 
we  know  that  the  nervous  system  is  more  relaxed  than  dur- 


TKEATMENT.  73 

ing  waking  hours,  consequently  these  persons  are  more  sus- 
ceptible to  the  exciting  causes  of  the  asthmatic  spasm  when 
they  are  asleep  than  when  awake,  and  the  paroxysm  comes 
on  soon  after  they  fall  asleep. 

By  whichever  class  of  remedial  agents  the  patient  is  re- 
lieved, after  a  time  the  remedy  which  has  given  relief  will 
fail,  or  cease  to  have  the  desired  effect ;  under  such  circum- 
stances, a  new  remedy  must  be  tried. 

The  three  most  reliable  remedies  are  ipecacuanha  as  a  de- 
pressant, opium  as  a  sedative,  and  coffee  as  a  stimulant. 

Compressed  air  has  been  recommended  as  of  great  ser- 
vice in  asthmatic  paroxysms.  I  have  never  found  pa- 
tients to  obtain  from  its  use  the  relief  promised  by  its 
advocates. 

As  a  rule,  inhalation  of  oxygen  gas  does  not  relieve  the 
paroxysms  of  asthma. 

During  the  intervals  the  treatment  must  be  altogether 
hygienic,  as  there  are  no  remedial  agents  the  use  of  which 
at  such  times  will  prevent  the  recurrence  of  the  paroxysms, 
while  the  observance  of  certain  hygienic  rules  will,  in  many 
cases,  prevent  their  return. 

Usually,  asthmatic  patients  are  dyspeptic  ;  and  it  is  a 
noticeable  fact  in  such  cases,  that  so  long  as  they  exercise 
proper  care  in  regard  to  their  diet,  they  are  free  from  attacks 
of  asthma.  This  is  a  fact  to  be  remembered  in  the  manage- 
ment of  a  patient  in  the  interval  between  the  paroxysms. 

A  change  of  residence  is  all -important  in  those  cases  which 
depend  for  their  development  upon  certain  atmospheric 
causes.  There  is  no  rule  which  can  be  observed  in  making 
this  change  of  residence  ;  each  patient  must  decide  for  him- 
self, finding  by  trial  in  what  place  he  is  free  from  his 
attacks. 

If  the  patient  is  anaemic  and  poorly  nourished,  cod-liver 
oil  and  iron  must  be  administered  during  the  interval.  I 
would  also  call  your  attention  to  the  use  of  quinine  during 
the  interval.  I  have  quite  a  number  of  asthmatics  under  ob- 
servation, who,  by  taking  daily  from  five  to  ten  grains  of 
quinine,  can  prevent  the  asthmatic  paroxysms ;  but  as 
soon  as  they  stop  its  daily  use,  their  asthmatic  symp- 


74  SPASMODIC   ASTHMA. 

toms  begin  to  manifest  themselves,  and  soon  culminate  in 
a  paroxysm. 

WHOOPING-COUGH. 

In  this  connection  I  am  compelled  to  say  a  few  words  to 
you  on  the  subject  of  whooping-cough,  for  although  this 
disease  strictly  should  be  classed  among  the  diseases  of 
children,  it  may  occur  at  any  age.  I  shall  therefore  give 
you  a  brief  account  of  it  as  one  of  the  bronchial  affections. 

MORBID  AXATOMY. — The  principal,  if  not  the  only  anato- 
mical changes  in  this  affection,  are  those  of  catarrhal  bron- 
chitis. Those  who  regard  the  disease  of  nervous  origin, 
claim  that  there  are  evidences  of  inflammation  of  the  vagus 
nerve,  or  congestion  of  the  medulla  oblongata ;  in  most 
cases,  however,  none  of  these  nervous  changes  can  be 
shown.  I  am  disposed  to  regard  it  as  a  peculiar  form  of 
catarrh  of  the  respiratory  mucous  membrane,  which  differs 
from  other  forms  of  catarrh  in  its  origin,  and  the  laryngeal 
and  bronchial  spasms  which  attend  its  development.  The 
complications  are  lobular  collapse,  lobular  emphysema, 
bronchial  dilatation,  and  catarrhal  pneumonia. 

ETIOLOGY. — It  is  an  infectious  disease,  which  depends 
upon  a  specific  poison  given  off  in  the  breath  of  the  person 
affected,  which  may  be  conveyed  a  considerable  distance. 
A  second  attack  is  scarcely  ever  observed.  The  period  of 
incubation  varies  from  five  days  to  two  weeks.  The  most 
common  complication  of  whooping-cough  is  capillary  bron- 
chitis, with  pulmonary  collapse  or  catarrhal  pneumonia. 

Whenever  the  coughing  fits  lose  their  characteristic  fea- 
tures and  become  dry  and  hacking,  and  the  dyspnoea  is 
greatly  increased  and  continues  through  the  intervals,  with 
a  marked  rise  in  the  temperature,  you  will  almost  certainly 
find  one  or  all  of  these  complications  present. 

Another  complication  which  is  particularly  to  be  feared 
in  the  progress  of  this  disease  is  cerebral  congestion.  When, 
during  a  paroxysm,  you  notice  the  countenance  flushed 
and  swollen,  the  jugular  veins  turgid,  with  a  gush  of  blood 
from  the  nose,  you  will  appreciate  the  danger  of  such  an 
occurrence. 


SYMPTOMS.  75 

When  you  find  the  face  habitually  flushed,  the  head  hot, 
the  patient  drowsy,  restless  in  his  sleep,  moaning  and  grind- 
ing his  teeth,  you  may  be  certain  if  these  symptoms  are 
allowed  to  continue,  that  convulsions  and  coma  will  soon 
be  developed,  and  the  disease  terminate  fatally. 

SYMPTOMS. — There  are  three  recognized  stages  in  whoop- 
ing-cough,— a  catarrhal,  a  spasmodic,  and  a  stage  of  decline. 

The  catarrhal  stage  commences  and  is  marked  by  the 
ordinary  symptoms  of  a  severe  naso-pharyngeal  and  bron- 
chial catarrh.  There  is  coryza,  and  usually  a  severe  parox- 
ysmal cough,  at  first  dry,  but  soon  it  is  attended  by  an 
abundant,  tenacious,  viscid,  transparent  mucus.  This  stage 
may  last  from  two  days  to  three  weeks. 

The  spasmodic  stage  is  marked  by  the  peculiar  charac- 
teristic spasmodic  cough,  from  which  the  disease  receives  its 
name. 

This  cough  is  very  severe  and  distressing  ;  it  begins  with 
a  long,  clear,  piping  inspiratory  sound,  followed  by  a  series 
of  rapid,  convulsive,  and  forcible  expiratory  puffs,  which 
are  succeeded  by  a  prolonged,  shrill,  inspiratory  sound,  or 
whoop.  If  the  fit  lasts  any  length  of  time,  the  cough  be- 
comes inaudible,  and  a  considerable  quantity  of  clear,  viscid 
mucus  is  expectorated  or  vomited  with  the  contents  of  the 
stomach.  During  the  paroxysm,  the  patient  grows  red  or 
purplish  in  the  face,  the  eyes  protrude,  the  tongue  assumes 
a  dark  appearance,  and  the  patient  seems  to  be  on  the  verge 
of  suffocation.  Bleeding  from  the  mouth,  nose,  and  ears 
often  occurs  during  a  violent  paroxysm.  The  subsidence 
of  the  paroxysm  is  usually  followed  by  a  sense  of  exhaus- 
tion, with  soreness  about  the  muscles  of  the  chest. 

A  physical  examination  of  the  chest  during  a  paroxysm 
of  whooping-cough  shows  a  feeble  or  absent  respiratory 
murmur  over  the  whole  chest,  with  sibilant  and  sonorous 
rales  ;  during  the  interval  mucous  rales  are  usually  heard. 

The  frequency  and  duration  of  the  paroxysm  varies 
greatly  in  different  cases.  As  a  rule,  the  more  violent  the 
paroxysm,  the  sooner  is  it  followed  by  another.  The  disease 
usually  attains  its  height  by  the  end  of  the  fourth  or  fifth 
week.  In  mild  cases  the  patient  is  well  in  the  interval  be- 


76  WHOOPING-COUGH. 

tween  the  paroxysms,  but  in  severe  cases  there  may  be 
languor  and  debility,  loss  of  appetite,  headache,  and  more 
or  less  fever. 

The  stage  of  decline  is  not  marked  by  any  sudden  transi- 
tion, but  a  gradual  diminution  in  the  frequency  and  severity 
of  the  paroxysms.  The  peculiar  whoop  ceases,  the  expec- 
toration is  less  difficult,  and  becomes  more  purulent  in 
character,  and,  finally,  after  a  period  of  about  nine  weeks, 
the  characteristic  cough  ceases  altogether,  and  the  patient 
passes  into  a  rapid  convalescence. 

DIFFERENTIAL  DIAGNOSIS. — In  its  earlier  stages,  it  is  not 
possible  to  diagnosticate  whooping-cough  with  certainty ; 
but  its  existence  may  be  suspected  if  the  cough  is  of  a 
violent  spasmodic  character,  if  the  fever  is  excessive  and 
prolonged,  and  if  the  disease  is  prevalent. 

When  the  disease  is  fully  established,  the  peculiar  cough 
and  expectoration  distinguish  this  affection  from  all  others. 

PROGNOSIS. — Whooping-cough  is  always  a  serious  dis- 
ease, although  it  is  rarely  directly  fatal ;  yet,  indirectly,  it 
frequently  causes  death.  It  is  dangerous  in  proportion  to 
the  number  and  severity  of  the  paroxysms,  the  intensity  of 
the  fever,  and  the  character  and  severity  of  the  complica- 
tions. A  fatal  result  is  generally  due  to  complications. 
Children  during  dentition,  sometimes  during  the  paroxysms 
of  the  coughing,  pass  into  convulsions,  which  are  generally 
fatal. 

A  condition  of  general  debility,  poverty,  and  destitution, 
a  residence  in  a  city  in  badly  ventilated  apartments,  and 
epidemic  influences,  tend  to  render  the  prognosis  unfavor- 
able. 

TREATMENT. — The  chief  indications  in  the  treatment  of 
whooping-cough  are  :  first,  to  diminish  the  severity  of  the 
paroxysms  ;  second,  to  prevent  and  treat  as  far  as  possible 
the  complications ;  third,  to  attend  to  the  general  health  of 
the  patient. 

There  are  no  known  means  by  which  this  affection  may 
be  averted.  The  paroxysms  cannot  altogether  be  pre- 
vented, but  their  severity  may  be  lessened.  All  of  the 
internal  and  external  specifics  for  the  prevention  of  the 


TREATMENT.  77 

paroxysms  of  whooping-cougli,  which,  have  been  proposed, 
and,  in  some  instances,  strongly  advocated,  are  of  very 
doubtful  benefit. 

The  most  important  and  reliable  remedies  for  relieving 
the  paroxysms  of  coughing  are  the  sedatives  arid  anti- 
spasm  odics,  the  most  efficient  of  which  are  belladonna, 
hydrocyanic  acid,  hyoscyamus,  cannabis  indica,  chloro- 
form, and  musk;  all  of  these  remedies  must  be  given  in 
minute  doses,  and  their  effects  closely  watched. 

The  diluted  mineral  acids — arsenic,  nux  vomica,  cochineal, 
bromide  of  potassium,  and  repeated  emetics — have  each  in 
turn  been  highly  recommended  as  specifics  for  the  control 
of  the  paroxysms  in  whooping-cough. 

Local  applications  to  the  larynx,  such  as  solution  of 
nitrate  of  silver,  etc.,  according  to  my  experience,  do  more 
harm  than  good  ;  and  the  same  is  true  of  counter-irritants, 
such  as  liniments  and  plasters. 

I  desire  to  impress  upon  you  the  fact,  that  whooping- 
cough  is  a  self -limiting  disease,  and,  like  all  other  diseases 
of  that  class,  must  be  treated  expectantly.  The  patient,  by 
warm  clothing,  should  guard  against  undue  exposure.  In 
bad  weather,  he  should  be  confined  to  the  house  in  a  room 
of  uniform  temperature ;  but  there  is  no  reason,  if  the 
weather  is  favorable,  why  he  should  not  go  out  into  .the 
open  air.  The  diet  should  be  simple,  and  the  state  of  the 
alimentary  canal  carefully  looked  after.  Adults  and  elder 
children  should  be  taught  to  suppress  the  cough  as  much 
as  possible. 

Complications  must  be  watched  for,  and  treated  as  soon 
as  they  occur.  Bronchitis  is  the  most  frequent  complica- 
tion ;  when  it  occurs  it  should  receive  prompt  attention, 
according  to  the  rules  already  given  for  the  management  of 
bronchitis,  great  care  being  taken  that  it  does  not  become  a 
broncho-pneumonia. 

If  the  symptoms  of  congestion  of  the  brain  or  of  pneu- 
monia are  developed,  they  should  be  met  by  the  most 
prompt  and  efficient  remedies  adapted  to  these  conditions, 
and  their  earliest  appearance  should  be  watched  for. 

It  is  important  to  remember  that  in  any  or  all  of  the  com- 


78  WHOOPIXG-COUGH. 

plications  of  whooping-cough,  the  treatment  should  be  sup- 
porting in  character. 

During  convalescence,  tonics,  such  as  iron,  quinine,  and 
cod-liver  oil,  are  indicated  ;  in  fact,  in  a  large  proportion  of 
cases  these  remedies  are  serviceable  throughout  the  whole 
course  of  the  disease. 

Sometimes  this  affection  assumes  a  chronic  form,  continu- 
ing after  several  relapses  much  beyond  the  usual  period. 
In  these  cases,  the  great  remedy  is  change  of  air. 

In  all  stages  of  whooping-cough,  benefit  is  derived  from 
a  short  sea-voyage,  and  a  temporary  residence  in  a  warm 
climate. 

It  has  been  recently  stated  by  some  very  judicious  ob- 
servers, that  large  doses  of  the  sulphate  of  quinine  have 
the  power  of  aborting  this  disease.  My  experience  in  this 
direction  is  not  sufficient  to  deny  or  sustain  the  statement ; 
but  my  impression  is  that  this,  like  all  other  so-called 
specifics,  after  a  more  extended  trial  will  be  found  un- 
availing. 


LECTURE 


PULMONARY  EMPHYSEMA. 

Vesicular  Emphysema. — Interlobular  Emphysema. 

CLOSELY  connected  with  the  two  diseases  which  have  just 
been  engaging  our  attention,  viz.,  bronchitis  and  asthma,  is 
pulmonary  emphysema,  for  you  will  seldom  meet  with  em- 
physema without  finding  it  associated  with  more  or  less 
bronchitis  ;  emphysematous  persons  are  especially  liable  to 
attacks  of  spasmodic  asthma.  Emphysema  is  essentially  a 
chronic  affection,  comes  on  slowly,  and  when  once  devel- 
oped is  permanent.  By  the  term  is  understood,  either  an 
abnormal  accumulation  of  air  within  the  air-cells,  or  an 
infiltration  of  air  into  the  subpleural  and  interstitial  con- 
nective tissue. 

There  are  two  recognized  varieties,  termed, — 

1st,  VESICULAR  EMPHYSEMA. 

2d,  INTERLOBULAR  EMPHYSEMA. 

The  first  is  by  far  the  more  frequent  and  more  important 
affection.  There  are  no  definite  rules  for  the  diagnosis  oi 
interlobular  emphysema,  and  it  rarely  occurs  except  in  con- 
nection with  advanced  vesicular  emphysema.  When  the 
unqualified  term  emphysema  is  used,  reference  is  always 
had  to  the  vesicular  variety. 

MORBID  ANATOMY. — In  emphysema,  there  maybe  simple 
dilatation  of  the  air-cells,  without  rupture  of  their  walls  ; 
or  there  may  be  dilatation  of  the  air-cells  with  rupture  of 
their  walls.  The  rupture  of  the  air-cells  leads  to  the  forma- 
tion of  what  may  be  called  air-sacs,  which  vary  in  size  from 
that  of  a  pin'  s-head  to  that  of  a  pigeon' s  egg,  and  even  larger. 
The  two  forms  of  the  affection,  the  vesicular  and  the  inter- 
lobular, are  generally  associated  with  these  larger  air-sacs. 


80  PULMONAKY   EMPHYSEMA. 

The  changes  which  take  place  in  the  anatomical  structure 
of  the  lung  in  this  affection,  are  as  follows  :  in  slight  cases, 
there  is  dilatation  of  the  cavity  of  the  infundibula,  and  a 
diminished  prominence  of  the  alveolar  walls,  followed  later 
by  their  rupture  and  partial  disappearance  ;  as  a  result,  a 
small  air-sac  is  formed,  in  which  little  ledges  and  filaments 
of  tissue  alone  mark  the  site  of  the  alveolar  septa.  As  the 
disease  advances,  the  walls  of  these  little  air-sacs  become 
ruptured,  and  in  this  manner  communication  is  established 
between  the  small  air-sacs.  The  openings  which  permit  the 
communication  between  air-sacs  are  at  the  very  central 
portion  of  the  sac,  where  is  found  the  thinnest  point  in  the 
wall ;  these  openings  gradually  enlarge,  until  a  number  of 
sacs  have  become  united  together,  when  one  large  air-cavity 
is  formed,  across  and  along  the  walls  of  which  exist 
remains  of  the  original  tissue.  These  larger  air-sacs  com- 
municate with  the  bronchi,  which  are  sometimes  enlarged. 

The  result  of  this  destruction  of  alveolar  septa,  is  a  loss  of 
the  capillary  plexus  in  their  walls, — for  the  capillary  plexus, 
which  normally  is  spread  over  the  walls  of  the  air-cells, 
gradually  disappears  with  the  loss  of  the  alveolar  septa.  At 
times  collections  of  fat  granules  are  seen  in  these  septa, 
whose  exact  position  is  undetermined,  whether  in  the  nuclei 
of  the  capillaries,  or  in  the  inter-capillary  cells,  probably  in 
both  ;  this  fatty  metamorphosis  follows  rather  than  pre- 
cedes the  dilatation,  and  is  not  constant. 

The  small  branches  of  the  pulmonary  artery  are  the 
longest  retained  ;  they  become  dilated,  looped,  and  com- 
municate by  anastomosis  with  the  pulmonary  vein,  and  thus 
the  circuit  of  the  pulmonary  circulation  is  kept  up, — but  it 
is  not  nearly  so  free  nor  abundant  as  that  which  exists  in 
the  normal  capillary  plexus.  The  pulmonary  circulation  is 
therefore  materially  interfered  with  by  this  structural 
change. 

Well-marked  emphysema  generally  affects  both  lungs  ;  it 
is  most  marked  in  the  upper  lobes,  especially  along  their 
anterior  borders.  Emphysematous  degeneration  through- 
out both  lungs  is  rare. 

If  the  emphysema  is  compensatory,  the  site  of  the  emphy- 


MORBID   ANATOMY.  81 

sema  will  vary  with  that  of  the  producing  cause.  When  it 
is  the  result  of  strong  pleuritic  adhesions,  it  most  frequently 
affects  the  anterior  border  of  the  lung  involved.  In  partial 
collapse  of  lung  from  obstructed  bronchi,  or  inexpansibility 
from  disease  of  its  structure,  usually  the  emphysema  will 
be  circumscribed  to  the  vicinity  of  the  bronchial  obstruc- 
tions or  the  structural  disease. 

When  emphysema  is  the  result  of  forced  inspiration  with 
closure  of  the  glottis,  as  occurs  in  violent  spasmodic 
croup,  etc.,  the  apex  and  anterior  borders  of  the  lung  are 
mainly  involved.  Emphysematous  lungs  do  not  collapse 
when  the  thoracic  cavity  is  opened. 

In  well-marked  cases,  the  lungs  meet  and  overlap  each 
other  in  the  medial  line.  The  left  overlaps  the  superficial 
cardiac  region,  both  extend  lower  than  normal,  and  the  heart 
is  pushed  downward  and  nearer  to  the  medial  line  than 
normal.  The  diaphragm  may  also  be  pushed  below  its  nor- 
mal position,  and  all  of  the  abdominal  viscera  crowded  out 
of  their  normal  position  in  consequence.  In  some  cases  the 
liver  has  been  so  displaced  as  to  lie  entirely  below  the  free 
border  of  the  ribs.  The  lungs,  when  removed  from  the  tho- 
racic cavity,  have  borne  the  impress  of  the  rib  as  furrows  on 
their  surface,  indicating  the  points  where  they  have  been 
pressed  against  the  ribs.  Indentations  made  by  pressure 
of  the  fingers  on  the  surface  of  the  lung  are  permanent, 
showing  a  loss  of  elasticity. 

The  dilated  alveoli  may  be  seen  at  times  on  the  surface 
of  the  lung  through  the  pleura,  or  on  section  may  be  found 
distributed  through  its  substance  ;  they  are,  however,  much 
more  apparent,  after  the  lung  has  been  blown  up  and  dried. 
When  the  air-sacs  are  large,  they  protrude  beyond  the  sur- 
face of  the  lung,  and  generally  have  a  globular  form ;  in 
some  cases,  they  seem  to  be  separated  by  a  neck  from  the 
rest  of  the  lung,  looking  like  appendages  to  it.  In  well- 
marked  examples  of  emphysema,  the  whole  anterior  sur- 
face of  the  lungs  may  be  covered  over  with  air-sacs,  com- 
pared sometimes  to  the  lungs  of  reptiles. 

The  color  of  an  emphysematous  lung  is  usually  abnor- 
mally pale :  it  feels  soft  and  cushion-like  to  the  touch  ;  it 
6 


82  PULMONARY  EMPHYSEMA. 

crepitates  but  little  when  pressed  between  the  thumb  and 
finger ;  it  sinks  in  water  less  readily  than  healthy  Jung- 
tissue,  for  though  its  volume  is  increased,  its  weight  is  di- 
minished. By  pressure  the  air  can  be  forced  out  of  the  larger 
and  smaller  sacs  into  the  bronchi.  The  evidences  of  bron- 
chitis are  usually  present  in  the  bronchial  tubes. 

The  parenchyma  of  the  lung  may  present  lesions,  which 
may  be  either  the  cause  or  a  complication  of  emphysema. 

Phthisis  and  pneumonia,  although  of  rare  occurrence, 
are  not  as  infrequent  as  many  writers  would  lead  us  to  sup- 
pose. As  a  rule,  in  advanced  cases  of  emphysema,  the  right 
heart  will  be  found  hypertrophied  and  dilated  ;  as  soon  as 
the  systemic  circulation  is  interfered  with,  the  left  ventricle 
becomes  hypertrophied,  and  this  hypertrophy  for  a  time 
will  compensate  for  the  obstruction  in  the  return  circulation, 
but  as  a  result  of  this  interference  when  long-continued, 
those  anatomical  changes  take  place  in  the  liver,  kidneys, 
and  spleen,  which  are  similar  in  character  to  those  which 
occur  in  connection  with  valvular  heart  lesions,  and  give 
rise  to  general  dropsy :  this  class  of  changes,  however, 
belong  to  the  remoter  lesions  of  emphysema. 

Senile  emphysema  differs  from  the  variety  which  I  have 
just  described  in  the  following  respects  :  the  lungs  are  not 
only  diminished  in  weight,  but  very  markedly  in  size  ;  the 
lobes  are  usually  united,  and  their  fissures  directed  verti- 
cally instead  of  horizontally,  the  lower  lobes  having  lost 
the  most  in  bulk ;  their  surface  is  irregular,  and  their 
structure  is  composed  of  enlarged  air-vesicles  and  sacs 
which  are  the  result  of  the  natural  atrophy  of  the  lung- 
tissue  which  takes  place  in  old  age. 

In  interlobular  emphysema  an  air-vesicle  or  sac  ruptures, 
so  that  air  escapes  into  the  interlobular  cellular  tissue, 
forming  sacs  of  large  or  small  size.  These  sacs  may  form 
beneath  the  pleura,  or,  extending  between  the  lobules  of  the 
lung  and  along  its  vessels,  reach  its  root,  and,  there 
spreading  in  the  mediastinal  cellular  tissue,  be  distributed 
over  the  neck  and  body.  The  size  of  the  air-sacs  beneath 
the  pleura  may  be  only  that  of  small  vesicles,  and  these 
limited  to  the  circumference  of  a  lobule,  or  they  may  reach 


ETIOLOGY.  83 

the  size  of  the  stomach.  They  may  be  distinguished  from 
the  vesicular  dilatations  by  being  movable  beneath  the 
pleura.  Perforation  of  the  pleura,  producing  pneumo- 
thorax,  is  a  rare  result  of  interlobular  emphysema. 

More  or  less  interlobular  emphysema  is  always  present 
in  advanced  vesicular  emphysema. 

ETIOLOGY. — The  causes  of  emphysema  may  be  divided 
into  primary,  secondary,  or  compensatory. 

Primary  emphysema  may  exist  independently  of  or  be 
associated  with  bronchitis.  Among  its  causes  are  forced 
expiratory  efforts,  the  glottis  being  closed  or  narrowed  as 
in  violent  coughing,  straining  at  stool,  etc.  In  a  few  rare 
instances  the  emphysematous  distention  is  produced  during 
strong  inspiratory  efforts.  In  both  instances,  the  disease  is 
developed  in  the  upper  lobes  of  the  lung.  Another  cause 
of  this  variety  of  emphysema  is,  that  there  exists  in  many 
persons  either  a  hereditary  or  an  acquired  impairment  of 
the  elasticity  of  the  lungs,  which  renders  them  more  readily 
dilatable  and  more  easily  torn.  There  are  three  prominent 
theories  which  have  been  advanced  to  account  for  this. 
First,  that  it  is  due  to  fatty  degeneration  of  the  alveolar 
walls  ;  but  this  fatty  degeneration  has  not  as  yet  been  de- 
monstrated. It  is  true  that  molecules  of  fat  are  seen  in  the 
remains  of  the  alveolar  septa,  but  they  are  the  result  rather 
than  the  cause  of  the  emphysema.  Second,  there  is  a 
theory  that  the  weakness  of  the  alveolar  walls  is  due  to  the 
growth  of  the  inter-capillary  nuclei.  Third,  that  it  is  due 
to  a  fibroid  degeneration  of  the  alveolar  septa.  None  of 
these  theories  have  as  yet  received  full  confirmation  from 
observers  ;  a  co-operation  of  all  of  them,  more  particularly 
of  the  last  two,  is  necessary  in  many  cases  to  satisfactorily 
explain  the  production  of  the  disease. 

Recently,  another  cause  for  the  development  of  this  form 
of  emphysema  has  been  advanced,  viz.,  an  abnormal  in- 
crease in  the  capacity  of  the  chest,  due  to  excessive  growth 
of  its  walls.  This  theory  as  yet  lacks  proof. 

The  causes  of  secondary  emphysema  are  conveniently 
considered  under  three  subdivisions,  in  all  of  which  the 
emphysema  is  best  denominated  compensatory. 


84  PULMONARY   EMPHYSEMA. 

The  first  of  these  subdivisions  comprises  all  cases  in  which 
the  emphysema  is  developed  around  small  portions  of  lung 
rendered  inexpansible  by  disease  of  its  tissue,  as,  for  exam- 
ple, lobular  collapse  from  obstruction  of  a  small  bronchus, 
— a  lobular  pneumonia, — a  pulmonary  infarction,  etc.  ;  the 
lobules  adjacent  to  those  that  are  thus  rendered  inexpansi- 
ble become  overdistended  by  a  forced  inspiration  or  a  forced 
expiration  during  a  violent  fit  of  coughing ;  some  would 
make  these  obstructions  operating  in  different  parts  of  the 
lung  a  primary  cause. 

A  second  subdivision  comprises  those  cases  where  a 
large  portion  of  lung,  either  from  some  internal  cause,  as 
pneumonia,  hypostasis,  atelectasis,  etc.,  or,  from  some  ex- 
ternal cause,  as  pleurisy,  etc.,  is  rendered  inexpansible, 
and  emphysema  is  developed  in  healthy  portions.  In  both 
of  these  subdivisions,  the  capacity  and  mobility  of  the  chest 
remaining  normal,  the  usual  and  especially  forced  inspira- 
tory  efforts  require  extra-distention  of  the  alveoli  to  com- 
pensate for  those  rendered  more  or  less  useless. 

A  third  subdivision  includes  those  cases  secondary  to 
croup,  whooping-cough,  pressure  on  the  trachea  or  main 
bronchi.  The  emphysematous  distention  in  this  class  of 
patients  is  produced  during  expiration. 

It  is  questionable,  however,  whether  compensatory  em- 
physema is  ever  developed  when  the  walls  of  the  air-cells 
have  not  been  enfeebled. 

Interlobular  emphysema  is  produced  by  forced  expira- 
tion with  narrowed  glottis,  as  during  severe  cough,  parturi- 
tion, straining  at  stool,  etc.  It  is  usually  preceded  by 
vesicular  emphysema.  It  may  also  occur  from  perforation 
of  the  lung  from  without,  as  in  fracture  of  the  ribs.  Senile 
emphysema  is  mainly  an  atrophy  of  the  lung  septa,  which 
become  obliterated,  so  that  the  vesicles  coalesce,  and  is  due 
to  impaired  nutrition,  which  affects  these  as  well  as  other 
organs  in  old  age. 

SYMPTOMS. — The  prominent  and  most  constant  objective 
symptom  of  emphysema  is  dyspnoea.  It  is  a  dyspnoea 
which  is  increased  by  physical  exercise,  by  the  occurrence 
of  fresh  attacks  of  bronchitis,  and  by  spasm  of  the  bronchi, 


SYMPTOMS.  85 

such  as  occurs  in  spasmodic  asthma.  When  the  emphy- 
sema is  well  marked,  very  slight  exertion  will  give  rise  to 
dyspnoaa  ;  when  the  emphysema  is  slight,  only  violent  ex- 
ertion will  be  followed  by  it.  It  is  mitigated  by  a  warm 
atmosphere,  and  returns  with  increased  severity  during  the 
cold  of  winter.  In  congenital  cases,  the  only  symptom 
during  childhood  and  early  adult  life  is  a  moderate  degree 
of  dyspmjea.  In  advanced  cases  of  the  disease,  the  dyspnoea 
is  liable  to  be  paroxysmal,  the  paroxysms  depending  upon 
a  tendency  to  spasm  which  emphysema  in  its  development 
seems  to  impart  to  the  bronchi.  A  cough  is  usually  pres- 
ent, but  it  is  due  to  bronchial  irritation,  and  unless  bron- 
chitis exists  the  cough  may  be  wanting.  The  expectoration 
varies  with  the  extent  and  character  of  the  accompanying 
bronchitis,  and  it  is  not  uncommonly  a  part  of  the  his- 
tory of  the  emphysema  ;  if  it  occurs  independent  of  the 
accompanying  bronchitis,  it  will  have  nothing  characteristic 
about  it. 

Usually  there  is  no  pain  in  the  chest  dependent  upon  the 
emphysema.  In  advanced  cases,  the  countenance  is  pecu- 
liar and  somewhat  characteristic  ;  it  is  of  a  dusky  hue,  and 
has  a  puffy  appearance,  which  contrasts  remarkably  with 
the  wasted  appearance  of  the  rest  of  the  body.  The  nos- 
trils are  distended,  thickened,  and  vascular,  and  expand 
with  each  inspiration  ;  the  angles  of  the  mouth  are  drawn 
downward,  the  voice  is  feeble,  the  patient  stoops  in  the 
act  of  walking,  and  his  whole  body  has  a  cachectic  appear- 
ance ;  the  capillary  circulation  of  the  extremities  is  mark- 
edly imperfect  on  slight  exertion. 

There  is  a  gradual  though  steady  loss  of  flesh  and 
strength. 

Usually,  the  disease  is  not  attended  by  febrile  excite- 
ment ;  the  pulse  is  not  accelerated,  but  is  markedly  feeble, 
and  the  temperature  of  the  body  is  below  the  normal  stan- 
dard. The  other  symptoms  observed  in  connection  with 
emphysema  are  indirect,  and  due  to  interference  with  the 
circulation.  Not  only  is  there  always  disturbance  of  the 
capillary  circulation  in  the  extremities,  but  the  face  and 
neck  will  present  a  fullness  or  even  a  turgidity  of  the  blood- 


86  PULMOXAEY   EMPHYSEMA. 

vessels  altogether  abnormal.  The  distention  of  the  jugular 
veins,  and  the  lividity  of  the  face  and  hands,  are  unquestion- 
ably due  to  the  interference  with  the  circulation  upon  the 
right  side  of  the  heart,  but  do  not  occur  until  that  stage 
is  reached  in  which  there  is  more  or  less  hypertrophy  and 
dilatation  of  the  right  ventricle.  Patients  who  have  reached 
this  stage  become  very  purple  in  the  face  after  and  during 
fits  of  coughing,  often  presenting  the  appearance  of  im- 
pending suffocation.  The  paroxysms  of  coughing  are  per- 
fectly characteristic  ;  an  attack  of  coughing  comes  on,  grows 
more  and  more  severe,  gathers  more  or  less  of  the  spasmodic 
element,  and  when  it  has  reached  its  climax  the  face  and 
hands  become  livid,  and  the  patient  is  completely  exhausted. 
Vertigo  is  a  common  symptom  in  advanced  emphysema ; 
it  is  most  apt  to  be  developed  during  a  fit  of  coughing,  and 
depends  upon  the  interference  with  the  return  circulation 
from  the  head. 

Emphysema  of  itself  does  not  give  rise  to  dropsy,  although 
in  advanced  cases,  the  feet  and  ankles  are  almost  always 
cedeniatous, — the  oadema  is  the  result  of  the  cardiac  or  renal 
complication.  Ordinarily,  there  is  more  or  less  disturbance 
of  the  digestive  organs  in  these  advanced  cases  ;  the  dis- 
turbance is  due  to  catarrh  of  the  stomach,  and  that  ca- 
tarrh is  the  result  of  a  passive  congestion  of  the  mucous 
membrane  of  the  stomach,  the  failure  of  the  right  heart. 

For  a  like  reason,  the  functions  of  the  kidney  are  more 
or  less  disturbed.  Emphysematous  patients  are  especially 
liable  to  hemorrhoids,  and  very  often  have  profuse  bleed- 
ings from  the  rectum. 

As  I  have  already  stated,  the  development  of  emphysema 
is  almost  always  slow, — in  rare  instances  it  is  developed 
with  rapidity,  and  is  then  called  acute.  If,  from  the  rational 
symptoms,  there  is  any  doubt  as  to  the  diagnosis  of  em- 
physema, the  doubt  will  disappear  when  you  resort  to  a 
physical  exploration  of  the  chest — for  the  physical  signs  in 
a  well-marked  case  are  characteristic. 

PHYSICAL  SIGNS. — By  inspection,  it  will  be  noticed  that 
there  are  alterations  in  the  shape  and  movements  of  the 
chest.  There  will  be  an  unnatural  elevation  of  the  sternum, 


PHYSICAL   SIG^S.  87 

as  if  from  congenital  deformity,  and  there  is  an  unnatural 
bulging  of  the  infra-clavicular  and  mammary  region,  which 
gives  to  the  chest  a  more  rounded  appearance  than  in  health ; 
this  has  been  termed  "barrel-shaped."  The  scapula  will 
be  brought  forward,  and  there  will  be  an  antero-posterior 
curvature  of  the  spine,  which  gives  to  this  class  of  patients 
a  stooping  posture  which  is  habitual.  The  muscles  of  the 
neck  are  unnaturally  prominent.  The  lower  portion  of  the 
chest  seems  contracted,  and  the  intercostal  spaces  are  wider 
above  than  below.  If  the  emphysema  is  extensive,  the 
apex  of  the  heart  will  be  found  beating  lower  down  than 
normal  and  more  towards  the  median  line  ;  if  the  right  side 
of  the  heart  is  extensively  dilated  there  will  be  an  epigastric 
impulse, — this  impulse  is  due  to  an  increase  in  the  size  of 
the  heart,  and  to  the  crowding  of  it  to  the  right,  and  lower 
down  in  the  thoracic  cavity. 

In  some  instances,  when  the  general  symptoms  of  em- 
physema are  well  marked,  the  lungs  are  atrophied  instead 
of  abnormally  dilated,  and  no  bulging  nor  prominence  of 
the  chest  (either  general  or  local)  occurs. 

The  movements  of  the  chest  walls  are  also  altered.  At 
the  upper  portion  expansion  on  inspiration  is  diminished 
or  entirely  wanting ;  the  whole  chest  moves  vertically  up 
and  down  with  inspiration  and  expiration,  as  if  it  were 
passively  lifted  from  the  shoulders,  and  composed  of  one 
solid  piece, — while  below,  the  chest,  instead  of  being  dilated 
with  inspiration,  is  contracted. 

The  respiratory  efforts  are  labored,  and  the  breathing  is 
chiefly  abdominal.  The  diaphragm  seems  to  be  more  ac- 
tively engaged  than  the  chest  walls  in  the  process  of  res- 
piration. 

In  cases  far  advanced,  the  existence  of  emphysema  can 
be  made  out  by  inspection  alone. 

On  palpation  the  vocal  fremitus  varies  ;  it  may  fall  be- 
low, or  equal,  or  it  may  exceed  that  in  health.  In  senile 
emphysema,  the  vocal  fremitus  is  usually  increased. 

The  intensity  of  the  percussion  sound  is  increased,  the 
pitch  is  lowered,  the  pulmonary  quality  of  the  sound  is 
greatly  diminished,  and  it  becomes  vesiculo-tympanitic — 


88  PULMONARY   EMPHYSEMA. 

that  is,  there  is  added  to  the  vesicular  element  a  tympa- 
nitic  quality  which  is  the  characteristic  percussion  sound 
of  emphysema,  and  is  not  met  in  connection  with  any  other 
pulmonary  disease.  The  percussion  note  is  not  materially 
affected,  either  by  forced  inspiration  or  by  forced  expira- 
tion. 

On  auscultation,  the  inspiratory  sound  is  either  short 
and  feeble,  or  actually  suppressed,  while  the  expiratory  is 
greatly  prolonged,  the  ratio  of  the  two  being  as  one  to  four 
instead  of  four  to  one. 

As  a  rule,  the  pitch  of  both  the  inspiratory  and  expiratory 
sound  is  lower  than  in  health.  In  some  cases  expiration  is 
lower  in  pitch  than  inspiration ;  in  other  cases  there  is  very 
little  difference. 

In  some  extreme  cases  of  emphysema,  the  respiratory 
sounds  are  of  equal  length,  greatly  exaggerated  in  intensity, 
and  of  a  harsh,  sibilant,  or  sonorous  quality,  the  harsh 
quality  undoubtedly  being  due  to  diminution  in  the  calibre 
of  the  minute  bronchial  tubes. 

In  some  cases,  when  interlobular  and  vesicular  emphy- 
sema are  combined,  a  crumpling  sound  is  heard,  which  has 
been  designated  as  the  "crumpling  sound  of  emphysema." 
This  sound  has  been  said  to  resemble  the  crepitant  rale,  but 
it  more  nearly  resembles  the  sound  of  crumpling  parchment 
than  the  crackling  sound  of  the  crepitant  rale.  The  vocal 
sounds  greatly  vary  ;  they  may  be  diminished,  or  altogether 
absent,  or  their  intensity  may  be  greatly  increased.  The 
heart- sounds  are  feeble. 

DIFFERENTIAL  DIAGNOSIS. — Slight  emphysema  cannot  be 
diagnosticated  with  certainty  ;  but  those  advanced  emphy- 
sematous  cases  which  give  rise  to  severe  dyspnoea  and  cya- 
nosis, are  readily  distinguished,  by  a  physical  examination 
of  the  thorax,  from  other  diseases  which  manifest  similar 
symptoms. 

The  disease  with  which  emphysema  is  especially  liable  to 
be  confounded  is  pneumothorax.  If  the  physical  signs  of 
the  two  diseases  are  properly  appreciated,  it  is  not  difficult 
to  distinguish  between  them.  In  emphysema,  the  percus- 
sion sound,  although  somewhat  tympanitic  in  character, 


DIFFERENTIAL  DIAGNOSIS.  89 

still  retains  a  pulmonary  quality,  and  there  is  a  vesicular 
element  to  the  respiratory  sound  ;  while,  in  pneumothorax, 
the  percussion  sound  has  a  well-marked  tympanitic  charac- 
ter, and  the  respiratory  sound,  if  audible,  is  amphoric  in 
character,  with  no  vesicular  element.  Emphysema  affects 
both  sides,  pneumothorax  only  one  side.  The  symptoms 
of  pneumothorax  come  on  suddenly,  while  those  of  emphy- 
sema are  slowly  developed,  and  never  are  so  urgent  as  those 
of  pneumothorax. 

A  diagnosis  of  compensatory  emphysema  may  not  be 
made  out  during  life,  but  the  fact  being  well  established 
that  it  does  almost  invariably  jexist  in  certain  conditions, 
the  probability  of  its  existence  should  always  be  borne  in 
mind  in  the  study,  examination,  and  treatment  of  those 
pulmonary  diseases  in  which  it  is  liable  to  occur. 

PROGNOSIS. — Emphysema  rarely,  if  ever,  directly  destroys 
life ;  but,  when  once  developed,  is  never  recovered  from, 
and  incapacitates  the  person  to  a  greater  or  less  degree  for 
active  exercise,  rendering  life  at  least  uncomfortable. 

It  strongly  predisposes  to  bronchitis,  and  renders  exist- 
ing bronchitis  more  severe.  Acute  bronchitis  of  the  smaller 
tubes  is  an  extremely  grave  affection  when  it  occurs  in  an 
emphysematous  person. 

Again,  emphysema  develops  heart-disease.  The  impedi- 
ment to  the  pulmonary  circulation,  which  exists  as  the 
result  of  the  emphysematous  changes  in  the  lung-substance, 
gives  rise  to  an  overloaded  state  of  the  right  cardiac  cavi- 
ties, which,  in  time,  leads  to  their  permanent  dilatation  and 
hypertrophy  of  their  walls ;  insufficiency  of  the  tricuspid 
valves  follows,  and  the  resulting  regurgitation  through  the 
tricuspid  orifice  into  the  right  auricle  causes  obstruction  to 
the  systemic  venous  circulation,  and  as  a  result  we  have 
congestion,  and  a  permanent  disturbance  of  the  function  of 
the  kidneys,  liver,  etc.  In  giving  a  prognosis  in  any  case 
of  emphysema,  the  liability  to  this  complication  should  be 
considered. 

Emphysema  also  predisposes  to  fatty  degeneration  of  the 
different  organs  and  tissues  of  the  body,  the  result  of  an 
impoverished  state  of  the  blood. 


90  PULMONARY  EMPHYSEMA. 

The  occurrence  of  these  secondary  affections  renders  em- 
physema a  serious  form  of  disease.  It  is  undoubtedly  a 
more  serioiis  aff ection  when  it  occurs  in  childhood  and  adult 
life,  than  in  old  age.  Once  thoroughly  established,  it  can- 
not be  cured. 

TREATMENT. — I  shall  briefly  consider  the  treatment  of  this 
affection  under  two  heads  :  first,  the  treatment  of  the  dis- 
ease itself ;  second,  the  treatment  of  secondary  changes  in 
other  organs,  which  changes  are  more  or  less  directly  induced 
by  the  emphysema. 

Accepting  the  view  that  the  changes  which  take  place 
in  this  disease  in  the  lung-tissue  are  the  result  of  im 
perfect  or  disordered  nutrition,  we  may  reasonably  expect 
that  by  improving  the  nutrition  the  progress  of  the  degen- 
eration may  be  checked  or  arrested,  and  perhaps  even  the 
elasticity  of  the  unaffected  portion  of  the  lung  may  be 
restored. 

The  most  rational  method  of  treatment  is  that  by  which 
we  aim  to  remedy  faulty  nutrition  in  other  organs  and  tis- 
sues. With  this  object  in  view,  the  drug  which  is  of  the 
greatest  service  is  iron.  This  remedy  should  be  taken  daily 
with  meals,  for  a  long  period,  by  persons  who  have  emphy- 
sema, or  in  whom  it  is  developing.  In  this  class  of  cases, 
the  preparation  which  I  prefer  is  the  etherial  tincture  of  the 
acetate  of  iron.  Sulphate  of  quinine  in  small  doses  may 
be  given  with  the  iron,  in  most  cases  with  benefit. 

Strychnia,  which  has  some  reputation  in  the  treatment  of 
this  disease,  I  am  confident  has  no  power  in  arresting  its 
development,  and  it  has  seemed  to  me  to  increase  the  fre- 
quency and  violence  of  the  paroxysms  of  dyspnoea,  and 
thus  to  hasten  rather  than  retard  the  emphysematous  devel- 
opment. 

If  an  emphysematous  patient  has  dyspeptic  symptoms, 
the  mineral  acids  in  combination  with  bitter  vegetable  infu- 
sions will  be  found  of  service. 

When  there  is  tendency  to  great  emaciation,  I  have  found 
cod-liver  oil  of  service.  Stimulants,  vinous  and  spirituous, 
when  taken  in  small  quantities  after  or  during  meals,  often 
give  beneficial  results,  and  whenever  their  use  is  followed 


TKEATMENT.  91 

by  marked  improvement  in  the  general  condition  of  the 
patient,  they  should  be  nsed  in  the  treatment  of  the 
disease. 

The  regulation  of  the  diet  and  the  general  management 
of  the  emphysematous  patient  is,  however,  of  much  greater 
importance  than  the  medical  treatment. 

The  diet  should  be  of  the  most  nutritious  character,  and 
composed  largely  of  animal  food, — overloading  the  stomach 
should  be  especially  avoided,  as  well  as  everything  which 
has  a  tendency  to  produce  flatulence.  The  food  should  not 
be  bulky  or  watery  in  character,  and  should  be  as  digesti- 
ble as  possible, — the  quantity  of  liquids  taken  into  the 
stomach  should  always  be  small.  Exercise  in  the  open  air 
should  be  taken  sytematically,  but  fatigue  should  be 
avoided.  All  violent  exercise,  or  great  physical  exertion, 
must  be  strictly  prohibited. 

Emphysematous  patients  should  not  expose  themselves 
to  cold.  All  localities  where  attacks  of  spasmodic  asthma 
are  liable  to  be  developed  should  be  carefully  avoided,  as 
also  anything  and  everything  which  may  develop  dyspnoea, 
or  predispose  the  patient  to  asthmatic  attacks. 

The  patient  should  live  in  the  open  air  as  much  as  possi- 
ble, and  in  such  conditions  as  will  secure  the  least  eifort  in 
respiration.  The  rule  for  all  emphysematous  persons  is,  to 
change  their  residence  to  that  locality  where  they  suffer 
least  and  are  not  troubled  with  dyspnoea. 

The  treatment  of  those  complications  which  accompany 
or  are  induced  by  the  emphysema,  is  also  of  importance  in 
arresting  the  progress  of  the  disease. 

Of  these  accompaniments,  bronchitis,  which  is  generally 
chronic  in  character,  stands  first.  In  addition  to  all  that 
can  be  accomplished  by  change  of  climate,  and  other  hygie- 
nic measures  in  the  management  of  that  form  of  bronchitis 
which  is  so  constant  an  accompaniment  of  emphysema, 
there  is  one  drug  which  I  have  found  especially  serviceable, 
viz.,  iodide  of  potassium.  It  should  be  given  in  doses  vary- 
ing from  five  to  twenty  grains,  three  times  during  the  day, 
and  its  administration  should  be  continued  at  intervals  for 
a  long  period. 


92  PULMONARY   EMPHYSEMA. 

With  regard  to  the  treatment  of  diseases  of  the  heart, 
liver  and  kidneys,  which  occur  as  complications  or  accom- 
paniments of  emphysema,  I  shall  consider  them  in  connec- 
tion with  the  history  of  cardiac  and  renal  diseases. 


LECTURE   VIII. 


PULMONARY  (EDEMA. 

Pulmonary  Congestion. — Pulmonary  Apoplexy. 

I  WILL  continue  the  study  of  abnormal  conditions  of  the 
respiratory  organs  by  inviting  your  attention  to  the  subject 
of  Pulmonary  (Edema. 

A  careful  examination,  immediately  preceding  death,  of 
the  lungs  of  a  large  number  of  persons,  proves  that  oedema 
of  the  lungs  is  of  far  more  frequent  occurrence  than  would 
be  readily  imagined.  It  is  generally  a  secondary  affection, 
—it  may  be  complicated  by  pulmonary  congestion,  or  it  may 
occur  independently  of  it. 

MORBID  AISTATOMY. — The  anatomical  lesion  of  pulmonary 
oedema  consists  in  the  presence  of  serum  in  the  cavity  of 
the  alveoli,  and  in  the  interstitial  tissue  of  the  lungs.  If  it 
is  associated  with  pulmonary  congestion,  the  serum  will  be 
blood-stained, — if  there  is  no  pulmonary  congestion  present, 
the  serum  in  the  cavity  of  the  alveoli  and  interstitial  tissue 
will  be  clear  in  color. 

Lungs  which  are  the  seat  of  pulmonary  oadema  do  not 
collapse  when  the  thoracic  cavity  is  opened.  Unless  conges- 
tion is  present,  that  portion  of  the  lung  which  is  the  seat 
of  the  oedema  is  paler  than  normal  lung-tissue.  When  the 
ffidematous  portion  is  pressed  upon  with  the  finger,  the 
indentation  remains,  showing  that  the  natural  elasticity  of 
the  tissue  is  diminished.  Its  weight  is  increased. 

On  section,  serum  exudes  or  can  easily  be  expressed  from 
the  cut  surface.  The  serum  is  usually  frothy ;  if,  however, 


94  PULMONARY   (EDEMA. 

the  air-cells  are  filled  with,  serum,  it  will  not  be  frothy  when 
section  of  the  lung- tissue  is  made.  It  is  by  this  means  we 
are  able  to  determine  the  amount  of  oedema  present. 
(Edema  may  occur  in  any  portion  of  lung-tissue,  but  it  is 
met  with  most  frequently  in  the  most  dependent  portion. 

When  O3dema  of  the  lungs  is  found  at  a  post-mortem 
examination,  it  is  impossible  to  decide  by  simple  inspection 
whether  it  occurred  before  or  after  death  ;  in  order  to  deter- 
mine its  exact  import,  it  is  necessary  to  know  the  physical 
signs  and  symptoms  present  previous  to  death. 

ETIOLOGY. —  Pulmonary  oedema,  as  has  already  been 
stated,  is  usually  a  secondary  affection. 

First. — It  may  be  caused  by  hydrsemia,  resulting  from 
general  dropsy,  depending  upon  Bright' s  disease,  scorbutus, 
purpura,  etc. 

Second. — It  occurs  in  portions  of  lung  which  are  the  seat 
of  pulmonary  congestion,  especially  when  the  congestion  is 
due  to  obstructed  circulation  through  the  heart. 

Third. — It  may  be  found  in  lung- tissue  which  is  adjacent 
to  parts  that  are  the  seat  of  inflammatory  or  irritative  pro- 
cesses, as  pneumonia,  capillary  bronchitis,  miliary  tubercu- 
losis, etc.  When  circulation  has  been  obstructed  in  one 
portion  of  the  lung  it  may  arise  in  another  portion  of  the 
same  lung ;  its  occurrence  in  connection  with  pneumonia 
is  not  infrequent  under  such  circumstances,  and  it  often 
becomes  a  most  alarming  complication,  demanding  prompt 
and  careful  attention  in  order  to  avert  its  fatal  tendencies. 

We  find  it  occurring  in  the  course  of  acute  general  dis- 
eases, such  as  typhoid,  typhus,  and  scarlet  fevers,  and  from 
feeble  heart' s  action,  especially  in  the  aged  and  feeble ; 
under  such  circumstances,  the  posterior  portion  of  the  lungs 
is  usually  the  seat  of  the  oedema,  and  its  production  is 
aided  by  gravitation. 

SYMPTOMS. — The  prominent  rational  symptoms  of  oedema 
of  the  lungs  are,  increased  frequency  in  the  respiration  and 
dyspnoea.  Frequently  the  dyspnoea  is  sudden  in  its  advent, 
and  extreme  in  its  character.  There  is  no  febrile  excite- 
ment. The  temperature  remains  normal.  The  pulse,  if  in- 
creased in  frequency,  is  feeble.  There  is  more  or  less  cough, 


DIFFERENTIAL  DIAGNOSIS.  95 

attended  by  a  watery  expectoration  which  is  colorless  un- 
less  pulmonary  congestion  is  present ;  then  it  is  more  or  less 
blood-stained.  If  the  oadema  is  extensive  or  if  it  compli- 
cates some  pulmonary  disease,  the  lips  become  blue,  the 
extremities  livid  and  cold,  and  the  patient  presents  a  more 
or  less  cyanotic  appearance. 

PHYSICAL  SIGNS. — The  signs  furnished  by  inspection  and 
palpation  are  negative.  There  is  more  or  less  dulness  on 
percussion  (never,  however,  complete)  over  the  seat  of  the 
oadema  ;  usually  the  dulness  is  equally  diffused  over  the 
posterior  surface  of  the  chest  on  both  sides,  and  is  most 
marked  at  the  most  depending  portion  of  the  lungs. 

On  auscultation,  the  respiratory  murmur  is  feeble,  some- 
times almost  entirely  absent,  or  harsh  and  coarse.  With 
inspiration  and  the  commencement  of  expiration,  small- 
sized  bubbling  rales  are  heard  over  the  seat  of  the  oedema. 
These  rales  are  sometimes  not  distinguishable  from  pneu- 
monic crepitation ;  generally  they  may  be  distinguished 
from  it  by  their  liquid  character.  The-  absence  of  any 
bronchial  character  to  the  respiratory  sound  excludes  the 
presence  of  pneumonic  consolidation.  Vocal  fremitus  and 
resonance  may  be  increased  or  diminished ;  both  are  quite 
unreliable  as  means  of  diagnosis. 

DIFFERENTIAL  DIAGNOSIS. — (Edema  of  the  lungs  may  be 
confounded  with  the  first  stage  of  pneumonia,  with  hydro- 
thorax,  and  with  capillary  bronchitis.  It  is  distinguishable 
from  pneumonia  by  the  absence  of  a  chill,  followed  by  fe- 
brile symptoms,  by  the  liquid  character  of  the  rales,  and  by 
its  occurrence  on  both  sides  at  the  most  depending  portion 
of  the  lungs.  A  patient  in  the  last  stage  of  Bright' s  dis- 
ease may  suddenly  develop  high  temperature  and  a  cough  ; 
but  in  such  a  case,  the  absence  of  the  chill,  as  well  as  the 
bubbling  character  of  the  rales,  will  enable  you  to  draw  the 
line  between  pneumonia  and  pulmonary  oedema. 

It  is  impossible  to  distinguish  pulmonary  oedema  from 
hydrothorax  by  the  objective  symptoms  alone  ;  the  physical 
signs  of  the  two  diseases  are  quite  distinctive.  On  physical 
examination  oedema  may  be  distinguished  from  hydrothorax 
by  the  presence  of  rales,  and  by  the  fact  that  the  level  of  dul- 


96  PULMOXAEY   OEDEMA. 

ness  is  not  changed  by  a  change  in  the  position  of  the  patient ; 
in  hydrothorax,  if  percussion  is  performed  while  the  pa- 
tient is  sitting  or  standing,  and  the  upper  border  of  the  dul- 
ness  is  marked,  direct  the  patient  to  stoop  forward,  and 
the  line  of  dulness  will  be  immediately  changed.  This  change 
in  the  level  of  the  fluid  at  once  settles  the  question  between 
oedema  and  hydrothorax. 

The  capillary  bronchitis,  from  which  pulmonary  redema 
is  to  be  distinguished,  from  its  commencement  is  almost  al- 
ways accompanied  by  fever.  The  expectoration  differs  in 
character  from  that  of  pulmonary  oedema. 

In  capillary  bronchitis  it  is  scanty  at  first  and  tenacious, 
and  when  the -disease  is  fully  established,  although  it  may 
be  abundant,  it  is  still  tenacious  ;  in  pulmonary  oedema  the 
expectoration  is  always  watery  in  character,  and  abundant. 
In  oedema  there  is  always  some  dulness  on  percussion,  often 
it  is  well  marked  ;  in  capillary  bronchitis  there  is  no  per 
cussion  dulness.  In  both  affections  the  rales  closely  resem- 
ble each  other ;  they  are  usually  more  abundant  in  capillary 
bronchitis  than  in  oedema.  The  two  diseases  are  liable  to 
occur  together,  but  the  presence  or  absence  of  fever,  and  the 
character  of  the  expectoration,  are  generally  sufficient  to  en- 
able you  to  make  a  correct  diagnosis. 

PEOGXOSIS. — This  mainly  depends  upon  the  condition  of 
the  patient  at  the  time  of  the  occurrence  of  the  oedema.  A 
large  number  of  persons  die  (often  suddenly)  from  pulmo- 
nary oedema  in  connection  with  general  dropsy;  especially  is 
there  danger  when  it  occurs  with  the  general  dropsy  depend- 
ing upon  renal  or  cardiac  disease.  When  one  lung  is  the 
seat  of  pneumonic  inflammation,  not  unf  requently  oedema  is 
suddenly  developed  in  the  other  lung,  and  so  destroys  life. 
In  continued  fevers,  phthisis,  and  other  exhausting  diseases, 
pulmonary  oedema  often  occurs  as  the  immediate  cause  of 
the  fatal  issue. 

Extensive  pulmonary  oedema,  sufficient  to  give  rise  to 
extreme  dyspnoea  and  a  cyanosed  condition  of  the  face  and 
extremities,  is  of  serious  import  and  should  not  be  lightly 
regarded  ;  it  necessitates  a  very  guarded  prognosis. 

TREATMENT. — The  treatment  of  this  affection  will  depend 


MOEBID   ANATOMY.  97 

almost  exclusively  upon  the  condition  with  which  it  is  asso- 
ciated. If  it  occurs  in  connection  with  Bright' s  disease 
the  excretory  function  of  the  kidneys  must  be  increased, 
and  the  vicarious  excretory  power  of  the  bowels  and  skin 
brought  into  active  operation  with  hydragogue  cathartics^ 
diuretics,  and  diaphoretics.  All  of  these  eliminating  forces 
must  be  crowded  to  their  utmost. 

Dry  cups  must  be  applied  over  the  thorax  and  lumbar 
region  as  often  as  the  patient  will  bear  their  application,  in . 
numbers  varying  from  twenty  to  fifty  at  each  application. 
If  it  occurs  in  connection  with  typhus  or  typhoid  fever, 
stimulants  are  indicated,  for  it  does  not  generally  make  its 
appearance  in  connection  with  these  diseases  until  symp- 
toms of  exhaustion  are  present. 

If  the  heart' s  action  is  feeble,  its  power  must  be  increased  ; 
under  such  circumstances  the  administration  of  digitalis 
will  be  of  service.  When  the  O3dema  occurs  in  connection 
with  pulmonary  congestion,  counter-irritation,  regulating 
the  heart's  action,  or  any  means  which  shall  have  a  ten- 
dency to  relieve  or  arrest  the  congestion,  should  be  em- 
ployed. 

In  those  diseases  in  which  there  is  feebleness  of  the  cir- 
culation and  depression  of  the  vital  powers,  it  is  important 
that  the  patient  should  not  lie  constantly  in  one  position. 
He  should  frequently  be  moved,  in  order  to  prevent  the 
gravitation  of  the  blood  to  the  most  dependent  portion  of 
the  lungs.  Care  must  also  be  taken  that  the  lungs  are 
emptied  as  frequently  and  fully  as  possible. 

PULMONARY  CONGESTION. 

Pulmonary  congestion,  or  hypersemia,  on  account  of  its 
close  connection  with  pulmonary  oedema,  should  be  con- 
sidered in  connection  with  it.  From  its  course,  it  may  be 
divided  into  active  and  passive.  Active  pulmonary  conges- 
tion occurs  with  violent  and  accelerated^action  of  the  heart. 
It  may  be  developed  in  young  persons  with  contracted 
chest,  by  violent  exercise,  like  running  or  jumping.  It 
may  be  developed  by  the  inhalation  of  too  stimulating  air  or 
gases,  such  as  an  atmosphere  surcharged  with  oxygen,  or 
7 


98  PULMONARY   COXGESTIO^. 

one  very  much  rarefied,  such  as  is  met  with  at  high  ele- 
vations. 

Passive  pulmonary  congestion  depends  upon  an  obstruc- 
tion to  the  return  circulation.     In  this  case,  the  fault  is ' 
with  the  veins.     In  active  congestion,  the  fault  lies  with  the 
arterial  circulation. 

Again,  pulmonary  congestion  may  be  divided,  with  regard 
to  its  amount  and  anatomical  character,  into  hyper  cemia ; 
splenization ;  hypostatic,  compensatory,  and  brown  indu- 
ration. Other  divisions  are  sometimes  made,  but  all  the 
varieties  which  you  will  meet  can  properly  be  classified 
under  one  of  these  heads. 

MORBID  ANATOMY. — When  the  congestion  constitutes 
hypersemia,  the  lungs  wholly  or  in  part  are  distended,  of  a 
dark-red  color,  crepitating  little,  and  are  heavier  and  less 
elastic  than  normal.  On  section,  dark  blood,  often  in  con- 
siderable quantity,  flows  freely  from  the  cut  surface,  but  the 
lung-tissue  still  retains  its  dark  color  on  account  of  the 
blood  remaining  in  the  capillary  vessels.  Pulmonary  hy- 
persemia may  be  active  or  passive  ;  it  is  simply  an  increased 
quantity  of  blood  in  the  capillaries  of  the  lung  :  this  may  be 
due  to  increased  force  in  the  heart' s  action,  or  to  obstruc- 
tion to  the  return  of  the  blood  to  the  heart,  or  to  local 
interference  with  the  pulmonary  circulation. 

Splenization  is  a  form  of  congestion  which  has  received 
its  name  from  the  close  resemblance  which  the  affected  por- 
tion of  lung-tissue  bears  to  the  spleen. 

The  portion  of  lung  which  is  the  seat  of  this  form  of  con- 
gestion is  of  a  darker  color  than  normal,  and  scattered 
throughout  its  substance  will  be  seen  little  red  or  yellowish- 
white  points ;  these  little  points  are  simply  blood  extrava- 
sations. 

Lung-tissue,  in  a  condition  of  splenization,  is  of  a  dark 
reddish-blue,  brown,  or  black  color,  airless,  firmer  than 
normal,  crepitates  less  freely,  has  a  more  uniform  homo- 
geneous appearance  upon  its  cut  surface,  and  is  less  moist 
than  normal  lung-tissue ;  a  dark  fluid  will  sometimes  ooze 
from  its  cut  surface,  but  not  so  freely  as  in  hypersemia,  and 
the  fluid  is  more  watery  in  appearance. 


MOKBID   ANATOMY.  99 

In  the  development  of  this  condition  of  lung-tissue,  we 
have  first  hypersemia,  then  interstitial  osdema  is  developed  ; 
it  is  this  interstitial  oedema  that  distinguishes  splenization 
from  hypersemia.  It  occurs  in  connection  with  typhoid  and 
typhus  fevers,  or  any  disease  in  which  there  are  certain 
blood  changes,  and  it  is  always  developed  slowly. 

Hypostatic  congestion  is  a  term  applied  to  that  form  of 
congestion  which  occurs  in  the  most  dependent  parts  of  the 
lung,  in.  persons  dying  of  diseases  which  have  confined  them 
in  bed  for  a  long  time.  It  very  closely  resembles  spleniza- 
tion, but  the  lung-tissue  does  not  have  that  doughy  feel 
which  is  present  in  splenization,  and  the  little  whitish  or 
reddish  points  which  are  seen  in  splenization  are  absent  in 
hypostatic  congestion. 

Compensatory,  or  collateral  congestion,  is  that  form  of 
congestion  which  occurs  in  one  portion  of  the  lungs,  due  to 
obstructed  circulation  in  so?ne  other  portion.  That  pul- 
monary congestion  in  unaffected  portions  of  the  lung  in 
pneumonia  and  pleurisy,  is  an  example  of  this  form.  The 
same  kind  occurs  in  collapsed  lung-tissue,  and  about  points 
of  venous  obstruction. 

JSrown,  or  pigment  induration.  This  form  of  congestion 
is  specially  connected  with  obstruction  or  regurgitation  at 
the  mitral  orifice.  The  lung  is  distended,  firm,  heavy, 
seldom  very  moist,  and  usually  contains  only  a  moderate 
amount  of  air.  It  is  dotted  with  yellowish  or  brownish 
spots,  usually  of  small  size,  whilst  its  own  color  is  generally 
red.  The  capillaries  of  the  lungs  are  exceedingly  enlarged, 
both  in  width  and  length,  and  encroach  on  the  lumen  of  the 
alveoli.  The  brown  or  yellow  spots  are  due  to  old  blood 
extravasations  which  have  undergone  granular  pigment 
degenerations ;  often  red  spots  from  recent  extravasations 
are  found  along  the  side  of  the  old  ones.  Some  parts  of  the 
lung  may  present  these  changes  very  markedly,  whilst 
others  are  but  little  affected.  Within  the  air-cells  are 
usually  found  large  cells  which  have  undergone  more  or 
less  pigmentation.  All  of  these  changes  result  from  an  in- 
terference with  the  return  circulation.  The  pigmentation 
which  is  present,  is  the  result  of  the  long-continued  reten- 


100  PULMONARY   CONGESTION. 

tion  of  blood  in  the  parts,  and  the  consequent  changes  in 
the  blood  itself. 

ETIOLOGY. — The  causes  of  the  different  varieties  of  pul- 
monary hemorrhage  I  have  sufficiently  considered  in  con- 
nection with  their  morbid  anatomy,  so  that  they  do  not 
require  a  separate  consideration. 

SYMPTOMS. — It  is  difficult  to  distinguish  the  symptoms  of 
pulmonary  congestion  from  those  of  pulmonary  O3dema, 
and  also  from  those  of  diseases  in  which  it  is  liable  to  occur 
as  a  complication.  If  the  congestion  is  considerable,  there 
is  more  or  less  dyspnoea,  cough,  and  expectoration.  Blood- 
stained watery  expectoration  is  the  prominent  objective 
symptom  of  pulmonary  congestion.  Dyspnoea  more  or  less 
marked  is  present  in  both  active  and  passive  congestion  of 
lungs.  The  dyspnoea  is  often  urgent  if  the  congestion  is 
extensive,  but  in  many  cases  of  passive  congestion  there 
will  be  little  change  in  the  respiration  ;  the  patient  becomes 
accustomed  to  habitual  dyspnoea  and  suffers  no  special  in- 
convenience except  moderate  shortness  of  breath  on  physi- 
cal exertion,  especially  is  this  the  case  in  brown  induration 
of  the  lungs, — a  feeling  of  tightness  or  oppression  is  often 
experienced  in  the  chest,  but  pain  is  rarely  present.  In  ex- 
treme cases  all  the  symptoms  which  attend  imperfect  aera- 
tion of  the  blood  are  developed,  and  the  patient  dies  as  in 
pulmonary  oedema. 

The  physical  signs  of  pulmonary  congestion  are  not  well 
marked  ;  the  movements  of  the  chest  are  increased  and  the 
respiration  more  or  less  labored  in  character.  The  percus- 
sion sound  is  at  first  abnormally  resonant,  but  as  oedema  is 
developed  in  the  congested  portion  and  in  brown  induration 
of  the  lung,  it  becomes  somewhat  dull. 

On  auscultation,  the  respiratory  murmur  is  feeble  or 
harsh, — in  brown  induration  of  the  lung,  there  is  a  feebleness 
of  the  normal  vesicular  murmur,  the  inspiratory  sound  be- 
comes harsh,  and  the  expiratory  becomes  prolonged.  Abun- 
dant small,  bubbling  rales  are  heard  when  oedema  accom- 
panies the  congestion,  as  is  almost  always  the  case  when  the 
congestion  is  active. 

DIFFERENTIAL  DIAGNOSIS. — The  diagnosis  of  pulmonary 


DIFFERENTIAL   DIAGNOSIS.  101 

congestion  is  not  very  difficult  if  you  take  into  account  the 
circumstances  under  which  it  occurs,  and  the  two  prominent 
symptoms,  viz.  :  the  dyspnoea,  and  the  copious,  watery, 
blood-stained  expectoration.  If,  therefore,  in  the  progress  of 
a  case  of  pneumonia,  watery  blood-stained  expectoration 
makes  its  appearance,  and  the  dyspnoea  is  increased,  pul- 
monary congestion  and  oedema  may  be  recognized  as  having 
been  added  to  the  pneumonia,  involving  that  portion  of 
lung  not  involved  in  the  pneumonia.  There  is  a  blood-stained 
expectoration  present  in  the  pneumonia,  but  it  is  of  a  tena- 
cious character,  and  entirely  unlike  the  copious,  watery, 
blood-stained  expectoration  of  the  pulmonary  congestion 
and  oedema.  The  existence  of  pulmonary  oedema  being  es- 
tablished, it  is  impossible  to  determine  whether  it  is  active 
or  passive  in  character  either  by  the  rational  or  physical 
signs  ;  but  in  the  majority  of  cases  the  circumstances  under 
which  it  occurs  will  decide  the  question. 

Pulmonary  congestion  is  readily  distinguished  from  spas- 
modic asthma  by  the  absence  of  the  characteristic  rales  of 
the  asthma. 

PROGNOSIS. — Active  pulmonary  congestion  is  usually  ra- 
pid in  its  course,  and  either  terminates  in  complete  recov- 
ery in  pneumonia  and  pulmonary  hemorrhage,  or  in  a  few 
hours  destroys  life.  Patients  suffering  from  the  disease 
can  generally  be  relieved  at  its  onset  from  the  dangers 
which  attend  it.  The  prognosis  in  passive  congestion  de- 
pends altogether  upon  the  condition  with  which  it  occurs. 
When  it  occurs  with  heart  disease  the  prognosis  will  vary 
according  to  the  exact  condition  of  the  heart ;  if  the  patient 
is  prostrated  from  heart  disease,  and  an  intense  pulmonary 
congestion  comes  on  suddenly,  the  prognosis  is  unfavorable  ; 
in  the  form  of  brown  induration,  the  prognosis  is  uncertain. 
Extensive  pulmonary  congestion  in  the  form  of  splenization 
leads  to  unfavorable  results.  As  a  rule,  pulmonary  con- 
gestion and  oedema  are  very  serious  affections,  because  they 
complicate  dangerous  conditions  already  existing. 

TREATMENT. — In  cases  of  active  congestion  coming  on  ab- 
ruptly, and  rapidly  assuming  a  threatening  aspect,  an  effort 
must  be  made  to  lessen  the  quantity  of  blood  in  the  pul- 

COLLIEGIE    LM  Ol-ATU 

I?K\  SlCL/vKt  KCLUK 


102  PULMONARY   APOPLEXY. 

monary  vessels  ;  this  is  best  accomplished  by  the  applica- 
tion of  wet  or  dry  cups  over  the  entire  chest,  or  over  the 
seat  of  the  congestion, — or  perhaps,  in  extreme  cases,  by  the 
opening  of  a  vein  in  the  arm  ;  these  remedies  to  be  followed 
by  steam  inhalations.  In  passive  congestion,  the  attention 
must  be  turned  to  the  condition  in  connection  with  which  it 
occurs,  and  by  overcoming  or  controlling  the  cause  of  the 
congestion,  regulate  the  pulmonary  circulation ;  if  it  de- 
pends on  feeble  heart's  action,  administer  stimulants  ;  if  on 
too  forcible  heart's  action  (the  organ  being  diseased),  give 
aconite  in  full  doses.  Hydragogue  cathartics  are  indicated 
when  it  is  associated  with  pulmonary  oedema. 

PULMONARY   APOPLEXY. 

We  pass  very  naturally  from  pulmonary  congestion  to 
pulmonary  apoplexy,  for  the  two  are  very  often  associated. 
There  are  two  recognized  varieties  of  pulmonary  apoplexy— 
the  circumscribed  and  the  diffused  ;  the  former  is  not,  while 
the  latter  is,  accompanied  by  laceration  of  the  parenchyma 
of  the  lung,  and  sometimes  the  laceration  is  extensive. 

MOPVBID  ANATOMY. — In  the  circumscribed  variety  the 
lungs  contain  a  variable  number  of  nodules,  termed  by 
recent  writers  hemorrhagic  nodular  infarctions ;  sometimes 
there  is  only  a  single  nodule,  rarely  many  of  them  ;  these 
are  of  dark  red  or  black  color,  they  contain  no  air,  are 
hard  or  soft  according  to  their  age,  and  are  easily  recog- 
nized by  their  firmness  when  pressure  is  made  on  the  por- 
tion of  lung  which  contains  them.  They  vary  in  size  from 
less  than  one  inch  to  four  inches  in  diameter ;  the  smaller 
are  the  more  frequent.  They  are  found  in  all  parts  of  the 
lung,  but  especially  in  the  posterior  portion  of  the  lower 
lobe  ;  not  unfrequently  they  protrude  from  the  outer  con- 
vex surface,  just  beneath  the  pleura.  After  these  nodules 
have  existed  for  a  considerable  time,  a  small  amount  of 
dark  grumous  blood  can  be  scraped  from  their  cut  surface  ; 
when  they  are  recent,  considerable  fluid  blood  can  be 
readily  pressed  from  their  cut  surface.  The  surrounding 
lung-tissue  forms  a  tolerably  well-defined  border,  and  may 
be  either  normal,  congested,  or  blood-stained. 

-   K  I-  \  G  [  ?  '.'  \J,  T 


MORBID   ANATOMY.  103 

As  a  rule,  these  nodules  are  formed  by  the  escape  of 
blood  from  the  capillaries  of  the  air-cells  into  the  cavity  of 
the  alveoli  and  minute  bronchi.  Some  of  it  is  retained  in 
these  cavities,  as  the  blood  after  its  escape  coagulates,  and 
the  capillaries  around  the  alveoli  are  also  filled  with  blood. 
There  is  no  rupture  of  lung-tissue.  Generally,  these  nod- 
ules are  wedge-shaped,  with  their  broad  extremities  towards 
the  surface  of  the  lung.  If  the  infarctions  occur  near  the 
surface  of  the  lung,  they  can  be  readily  recognized  through 
the  pleura,  by  their  dark  color,  and  also  by  the  fact  that 
the  lung  around  them  collapses,  giving  rise  to  little  promi- 
nences upon  their  surface. 

These  nodules  may  undergo  a  variety  of  changes.  Reso- 
lution is  the  most  frequent  change,  which  takes  place  as 
follows :  as  soon  as  the  blood  has  been  extravasated  into 
the  air-cells,  it  coagulates  and  is  of  a  dark  red  color,  it  soon 
changes  to  a  brown,  and  then  to  a  light  gray  color,  the 
fibrin  becomes  granular,  the  blood  globules  fatty,  and  their 
pigment  is  converted  into  hsematoidine  and  melanine. 
When  these  changes  have  taken  place,  the  infarction  is  in 
a  condition  either  to  become  absorbed  or  expectorated, 
usually  there  is  left  behind  a  pigmented  stain  to  mark  the 
former  situation  of  the  infarction  ;  after  a  time  air  may  re- 
enter  the  air-cells.  At  post-mortem  examinations  these 
pigmented  spots  are  frequently  seen  long  after  the  disap- 
pearance of  the  infarction  ;  after  a  time  air  re-enters  the  air- 
cells.  As  a  second  result  these  infarctions  may  remain  as 
dark,  pigmented,  cicatricial  spots,  impermeable  to  air  and 
sometimes  containing  calcareous  or  cheesy  products. 

In  the  third  place,  these  infarctions  may  excite  inflamma- 
tion of  a  pneumonic  character  in  the  surrounding  lung- 
tissue,  which  inflammation  may  terminate  in  gangrene,  or 
the  nodules  may  become  gangrenous  themselves.  The 
pleura  over  the  superficial  nodules  is  usually  coated  with 
recent  lymph. 

When  these  infarctions  occur  in  connection  with  pyaemia 
or  in  a  condition  corresponding  to  it,  their  tendency  is  to 
terminate  in  gangrene  or  in  the  formation  of  abscess.  The 
exciting  cause  of  the  inflammatory  process  which  is  to  ter- 


104  PULMONARY  APOPLEXY. 

minate  in  gangrene  or  the  formation  of  abscess  exists  in  the 
embolus  which  gives  rise  to  the  infarction,  its  character  is 
such  as  will  cause  suppuration  to  take  place  in  the  tissues, 
wherever  it  becomes  lodged.  In  the  diffused  varieties  of 
pulmonary  apoplexy  the  lung-tissue  becomes  torn  and  infil- 
trated with  blood,  which  may  be  either  fluid  or  coagulated. 
If  situated  near  the  surface  of  the  lung  the  pleura  may  be 
lacerated.  Generally,  the  cavity  made  in  the  lung-tissue  by 
the  extravasation  is  of  considerable  size,  and  the  coagulated 
or  semi-coagulated  blood  in  this  cavity  has  all  the  charac- 
teristics of  a  blood-clot.  These  apoplectic  extravasations 
are  never  circumscribed,  and  are  usually  of  much  larger 
size  than  the  circumscribed  variety.  They  may  prove  im- 
mediately fatal,  especially  when  the  pleura  is  perforated. 

If  the  patient  survives  the  shock  of  the  accident,  recovery 
usually  takes  place,  either  by  adhesion  of  the  torn  surfaces 
of  the  lung  after  absorption  of  the  extravasated  blood,  or  a 
connective-tissue  capsule  may  be  formed  around  the  clot, 
after  which  it  undergoes  a  cheesy,  cretaceous,  or  pigmented 
degeneration,  and  remains  permanently  imbedded  in  the 
lung-tissue.  This  form  of  apoplexy  is  much  less  frequently 
met  with  than  the  circumscribed  form. 

ETIOLOGY.  —  Pulmonary  infarction  may  be  caused  by 
anything  which  shall  obstruct  a  pulmonary  artery  or  pul- 
monary vein,  and  under  all  circumstances  it  is  embolic  or 
the  result  of  thrombosis. 

As  a  rule,  an  embolus  coming  from  some  other  part  of 
the  body  plugs  up  a  small  branch  of  the  pulmonary  artery, 
and  the  capillary  vessels  beyond  undergo  distention  from 
collateral  fluxion,  blood  escapes  from  the  capillaries  into 
the  cavity  of  the  alveoli  and  undergoes  coagulation,  and  a 
nodule  is  formed  corresponding  in  .size  to  the  space  occupied 
by  the  capillaries  which  are  the  termination  of  the  obstruct- 
ed artery.  The  embolus  may  have  come  from  the  right 
side  of  the  heart  as  a  consequence  of  an  endocarditis,  or 
from  a  coagulum  formed  in  the  right  heart,  the  result  of 
feeble  heart  action,  or  from  a  coagulum  formed  in  a  super- 
ficial vein  in  some  remote  part  of  the  body.  Any  foreign 
substance  of  sufficiently  small  size,  and  in  a  condition  in 


SYMPTOMS.  105 

which  it  shall  not  undergo  changes  when  introduced  into 
the  general  circulation,  may  find  its  way  into  a  branch  of 
the  pulmonary  artery  and  give  rise  to  a  pulmonary  infarc- 
tion. 

Nodular  hemorrhagic  infarctions  are  rarely,  if  ever,  pro- 
duced by  a  penetration  of  blood  from  the  mouth,  larynx, 
or  bronchial  tubes  into  the  air-cells.  Independent  of  pyae- 
mia and  cardiac  disease,  they  have  been  met  with  in  a  few 
other  conditions,  as  phthisis,  scorbutus,  cholera,  etc.  An 
artery  or  vein  may  in  more  instances  be  occluded  by  a 
thrombus  formed  subsequent  to  the  apoplexy. 

Diffused  pulmonary  apoplexy  may  occur  from  a  very 
large  infarction,  but  that  is  comparatively  rare.  It  gene- 
rally occurs  as  a  result  of  changes  in  the  walls  of  the  arte- 
ries. The  pulmonary  artery  may  be  the  seat  of  aneurism 
usually  of  small  size ;  or  it  may  occur  in  connection  with 
aneurism  of  some  other  vessel — as  the  aorta,  which  has  rup- 
tured into  the  lung  substance.  It  may  occur  as  the  result 
of  a  fall  or  shock ;  it  may  also  be  of  traumatic  origin, 
resulting  from  fracture  of  the  ribs,  gunshot  wounds,  etc. 
Its  most  frequent  cause  is  the  rupture  of  thoracic  aneu- 
risms. 

SYMPTOMS. — In  speaking  of  the  symptoms,  I  shall  limit 
myself  to  two  circumstances  under  which  apoplexy  may 
occur,  viz. :  with  cardiac  disease  and  with  pyaemia. 

When  pulmonary  apoplexies  occur  in  connection  with 
cardiac  disease,  and  are  few  in  number,  every  symptom  of 
their  occurrence  will  be  absent  except  one,  and  that  is  an 
expectoration  of  small  blood  coagula. 

If,  however,  the  infarction  is  of  considerable  size,  or  if  a 
number  of  infarctions  occur  at  the  same  time,  very  decided 
symptoms  will  mark  their  occurrence ;  prominent  among 
these  is  the  sudden  occurrence  of  severe  dyspnoea.  The 
patient  may  have  been  subject  to  mild  attacks  of  cardiac 
dyspnoea,  but  the  dyspnoea  from  which  he  now  suffers  is 
of  a  peculiar  character ;  it  is  usually  attended  by  a  sensa- 
tion of  constriction  about  the  chest,  and  he  is  aware  that 
Borne  extensive  damage  has  suddenly  been  done  to  his 
lungs.  If  the  infarction  occurs  near  the  pleura  there  will 


106  PULMONARY  APOPLEXY. 

be  pain  in  the  side  over  the  affected  lung,  the  result  ol 
pleurisy  over  the  infarction. 

The  development  of  pulmonary  infarctions  in  connection 
with  cardiac  disease  is  preceded  by  some  disturbance  of 
the  heart's  action.  The  patient  has  been  under  strong  men- 
tal excitement  or  has  made  too  violent  physical  exertions. 
Occasionally,  for  some  time  previous  to  the  infarction,  with- 
out any  apparent  cause,  the  heart' s  action  becomes  irregular, 
which  permits  the  formation  of  a  coagulum  in  its  cavity, 
and  the  breaking  up  of  this  coagulum  furnishes  the  emboli 
which  cause  the  infarction.  In  one  who  has  cardiac  dis- 
ease, an  irregular  and  intermitting  action  of  the  heart,  fol- 
lowed by  sudden  dyspnoea  and  a  dark  bloody  expectora- 
tion, are  very  certain  signs  of  the  occurrence  of  pulmonary 
infarction. 

Pulmonary  oedema,  congestion,  bronchial  hemorrhage, 
and  infarction  may  all  be  developed  together  ;  the  charac- 
ter of  the  expectoration  is  the  leading  feature  in  their  dif- 
ferential diagnosis.  In  bronchial  hemorrhage  the  expec- 
torated blood  is  of  a  bright-red  color,  in  pulmonary  oedema 
and  congestion  it  is  a  bloody  serum,  and  in  pulmonary 
infarction  it  contains  small  dark  blood-clots. 

PHYSICAL  SIGNS. — When  the  infarctions  are  of  large  size, 
their  seat  may  sometimes  be  determined  by  physical  exam- 
ination of  the  chest.  There  will  be  dulness  on  percussion, 
and  either  absence  of  respiratory  murmurs  or  of  bronchial 
respiration  over  the  region  which  is  the  seat  of  the  infarc- 
tion. The  existence  of  circumscribed  dulness  and  bronchial 
respiration,  in  connection  with  the  rational  symptoms 
already  referred  to,  is  usually  quite  sufficient  to  determine 
the  existence  and  seat  of  pulmonary  apoplexy  of  the  cir- 
cumscribed variety. 

The  development  of  that  form  of  pulmonary  infarction 
which  occurs  in  connection  with  pyaemia  (also  called 
metastatic  infarction)  is  marked  by  a  rapid  rise  in  tempera- 
ture, by  extreme  dyspnoea,  and  by  the  peculiar  blood-clot 
expectoration  already  referred  to. 

The  symptoms  which  mark  the  occurrence  of  diffused 
pulmonary  apoplexy  are  usually  not  well  defined,  and  it 


PULMONARY   APOPLEXY.  107 

may  be  difficult  positively  to  determine  its  existence. 
There  may  be  a  profuse  hemorrhage  with  the  development 
of  extensive  pneumonic  consolidation,  but  this  will  not 
distinguish  it  from  other  profuse  pulmonary  hemorrhages. 
This  form  of  apoplexy  often  goes  unrecognized  until  the 
post-mortem  examination. 

PROGNOSIS. — In  slight  circumscribed  pulmonary  apoplex- 
ies, depending  upon,  or  accompanying  heart  disease,  or 
occurring  in  connection  with  any  condition  that  is  not 
pysemie,  the  prognosis  is  good, — they  usually  go  on  to 
recovery,  excepting  a  slight  damage  to  the  lung-tissue  at 
the  point  of  the  hemorrhage.  The  majority  of  patients  who 
have  chronic  heart  disease  at  times  have  hemorrhagic  in- 
farction. All  hemorrhages  that  occur  in  connection  with 
pyaemia,  or  in  connection  with  thrombosis,  render  the  prog- 
nosis bad. 

TREATMENT. — The  treatment  of  pulmonary  apoplexy  is 
almost  entirely  expectant. 

If  it  results  from  heart  disease,  all  depressants,  such  as 
blood-letting,  etc.,  must  be  avoided.  The  main  thing  to  be 
accomplished  under  these  circumstances  is  to  regulate  the 
heart's  action  and  increase  its  force.  This  can  be  best  ac- 
complished by  the  moderate  use  of  stimulants  and  the  ad- 
ministration of  digitalis  in  full  doses.  It  is  also  all-impor- 
tant that  the  patient  should  be  kept  in  bed,  and  absolute 
quiet  should  be  enjoined.  Stimulating  applications  must 
be  made  to  the  extremities,  such  as  mustard  sinapisms,  and 
free  dry-  cupping  to  the  surface  of  the  chest  is  of  the  utmost 
importance.  Haemostatic  remedies  are  rarely  if  ever  required. 

If  inflammation  of  the  lung  or  pleura  follow  the  infarc- 
tion, it  must  be  treated  the  same  as  pneumonia  or  pleurisy 
occurring  under  any  other  circumstances. 

When  pulmonary  apoplexy  occurs  in  connection  with 
pyaemia,  the  treatment  consists  in  supporting  the  patient 
by  the  administration  of  stimulants,  quinine  and  iron,  and 
the  frequent  application  of  dry  cups  over  the  surface  of  the 
chest.  The  diffused  variety  of  pulmonary  apoplexy  is  not 
amenable  to  treatment. 


LECTURE  IX, 


BRONCHIAL  HEMORRHAGE. 

Gangrene  of  the  Lungs. — Cancer  of  the  Lungs. 

I  WILL  this  morning  continue  the  history  of  hemor- 
rhages from  the  respiratory  organs,  by  inviting  your  atten- 
tion to  the  subject  of  bronchial  hemorrhages. 

In  the  majority  of  instances,  when  blood  is  expectorated 
in  considerable  quantities,  the  seat  of  the  hemorrhage  is  the 
bronchial  mucous  membrane.  As  I  stated  to  you  in  my 
last  lecture,  spitting  of  blood  is  present  in  pulmonary  con- 
gestion, pulmonary  apoplexy,  and  in  the  inflammatory  pro- 
cesses affecting  the  lungs  and  bronchi ;  but  hemorrhage  from 
the  bronchial  tubes  is  by  far  the  most  frequent  cause  of 
spitting  of  blood,  or  TicEmoptysls. 

MORBID  Aisr ATOMY. — If  the  bronchial  mucous  membrane 
is  examined  soon  after,  or  during  a  bronchial  hemorrhage,  at 
the  seat  of  the  hemorrhage,  it  will  be  found  swollen,  relaxed, 
bleeding  on  slight  pressure,  and  of  an  uniformly  dark-red 
color,  with  here  and  there  spots  of  ecchymosis.  If  the  ex- 
amination is  made  some  time  after  the  bleeding,  the  bron- 
chial membrane  will  either  present  a  pale  and  bloodless  ap- 
pearance, or  no  traces  of  the  seat  of  the  hemorrhage  can  be 
found.  If  the  examination  is  made  during  or  soon  after  the 
hemorrhage,  at  points  the  bronchi  may  be  found  more  or 
less  completely  filled  with  blood-clots ;  these  clots  usu- 
ally are  exsanguinated.  If  the  blood  has  been  forced  from 
the  bronchi  into  the  air-cells,  small,  red,  dense  nodules  will 
be  found  scattered  through  the  lung-substance,  very  closely 


BEOSTCHIAL   HEMOEEHAGE.  109 

resembling  in  their   gross  appearance  pulmonary  infarc- 
tions. 

If  any  of  the  small  bronchi  are  completely  occluded  by 
blood-clots,  the  lung-tissue  beyond  the  seat  of  the  plugs 
will  remain  inflated  after  the  thoracic  cavity  is  opened. 
Ulceration  of  the  bronchial  mucous  membrane  is  rarely,  if 
ever,  a  source  of  bronchial  hemorrhage. 

ETIOLOGY. — The  two  prominent  causes  of  bronchial  hem- 
orrhage are,  first,  over-distention  of  the  capillaries  of  the 
bronchial  mucous  membrane ;  second,  weakness  of  the  ca- 
pillary walls  of  the  bronchial  membrane.  Such  weakness 
of  the  walls  of  the  capillaries  may  be  a  hereditary  or  an 
acquired  condition. 

The  tendency  to  bronchial  hemorrhage  from  weakened 
capillaries  is  much  stronger  between  the  ages  of  fourteen 
and  thirty,  especially  in  young,  delicate  persons  born  of 
phthisical  parents,  than  in  any  other  class.  There  is  also 
strong  predisposition  to  this  form  of  hemorrhage  in  persons 
who  are  already  suffering  from  developed  phthisis,  or  who 
have  an  acquired  phthisical  diathesis.  Usually,  in  this 
class  of  cases,  the  direct  cause  of  the  hemorrhage  is  a  sud- 
den distention  of  the  weakened  bronchial  capillaries  from 
violent  physical  exertion,  or  from  certain  peculiar  atmo- 
spheric influences.  In  rare  instances,  it  occurs  without  any 
appreciable  cause.  That  form  of  bronchial  catarrh  which 
precedes  or  attends  the  development  of  catarrhal  phthisis  is 
very  frequently  preceded  or  attended  by  bronchial  hemor- 
rhage. In  this  class  of  cases,  probably  the  exciting  cause 
of  the  hemorrhage  is  acute  hypersemia  of  the  bronchial 
membrane.  Bronchial  hemorrhage  may  be  induced  by  the 
inhalation  of  irritating  gases  or  vapors,  and  by  the  rarefied 
air  of  high  elevations  ;  in  both  of  these  instances,  the  hemor- 
rhage follows  over-distention  of  the  capillary  vessels  of  the 
bronchial  membrane. 

SYMPTOMS. — The  symptoms  which  attend  a  bronchial 
hemorrhage  vary  with  the  amount  of  the  hemorrhage.  If  the 
quantity  of  blood  expectorated  is  very  small,  no  symptoms 
will  be  developed  except  the  spitting  of  the  blood,  which 
is  of  a  bright-red  color.  It  is  not  often,  however,  that  the 


110  SYMPTOMS. 

symptoms  that  attend  a  bronchial  hemorrhage  are  so  trivial, 
for  these  hemorrhages  are  usually  profuse.  All  bronchial  hem- 
orrhages are  attended  by  the  spitting  of  bright-red,  frothy, 
arterial  blood,  and  it  is  to  this  form  of  hemorrhage  we  gen- 
erally allude  when  we  use  the  unqualified  term  licemoptysis. 

A  very  profuse  bronchial  hemorrhage  may  come  on  sud- 
denly without  any  warning,  but  usually  the  patient  has 
had  some  previous  indication  of  its  occurrence,  such  as  a 
sense  of  constriction  at  the  upper  portion  of  the  chest,  or, 
upon  respiration,  a  sense  of  uneasiness  which  he  cannot 
account  for.  He  may  or  may  not  have  had  a  cough  pre- 
ceding the  hemorrhage, — suddenly,  he  feels  as  if  some  fluid 
had  commenced  trickling  under  the  sternum,  and  he  notices 
an  unnatural  sweetish  taste  in  his  mouth,  he  spits  and  finds 
that  the  fluid  is  blood,  although  there  may  have  been  no 
cough  previous  to  the  hemorrhage  ;  now  he  feels  more  or  less 
bronchial  irritation,  which  is  followed  by  a  cough,  more  or 
less  blood  is  expectorated,  short  intervals  occur  between 
the  fits  of  coughing,  and  in  this  way  blood  may  continue  to 
be  expectorated  for  several  days,  or  the  expectoration  may 
continue  only  for  a  few  hours.  The  amount  of  blood  ex- 
pectorated varies  ;  sometimes,  when  the  hemorrhage  is  pro- 
fuse, the  whole  quantity  may  reach  a  pound  or  more  ;  at 
other  times  not  more  than  an  ounce  or  two  is  expectorated. 

During  the  occurrence  of  the  hemorrhage,  the  counte- 
nance of  the  patient  assumes  a  pale,  anxious  expression ; 
he  becomes  tremulous,  and  often  faints  ;  this,  however,  is 
not  owing  to  the  loss  of  blood,  but  is  probably  due  to  the 
shock  to  the  nervous  system  from  the  sight  of  blood,  and 
knowledge  of  the  fact  that  a  hemorrhage  from  the  lungs 
has  taken  place.  All  of  these  symptoms  may  be  present 
when  the  individual  has  not  lost  more  than  half  a  pound  of 
blood.  It  has  been  said  that  hemorrhage  from  the  lungs 
weakens  a  patient  more  than  hemorrhage  from  any  other 
organ  of  the  body. 

After  the  profuse  expectoration  of  blood  has  ceased,  the 
patient  goes  on  coughing  for  a  few  days,  expectorating 
small,  dark,  coagulated  masses  of  blood,  or  blood-streaked 
sputa.  Sometimes  bronchial  hemorrhage  is  so  profuse  that 


BRONCHIAL  HEMORRHAGE.  Ill 

the  blood  spouts  out  of  the  mouth  and  nose,  this  is  followed 
by  nausea  and  vomiting  of  blood  ;  but  it  is  worthy  of 
notice  that  the  nausea  and  bloody  vomiting  follow  and  do 
not  precede  the  hemorrhage.  Attacks  of  bronchial  hemor- 
rhage are  rarely  single,  usually  for  a  week  or  two  they  recur 
at  intervals  ;  at  length  the  patient  becomes  pale  and  feeble, 
then,  gradually,  recovery  takes  place,  so  that  in  a  few 
weeks  he  may  feel  even  better  than  before  the  hemorrhage  : 
this  is  the  most  favorable  termination  that  can  be  hoped 
for,  except  in  those  cases  in  which  the  hemorrhage  is  com- 
paratively insignificant. 

It  is  important  for  you  to  remember  that  attacks  of 
bronchial  hemorrhage,  however  profuse,  generally  are  re- 
covered from,  in  spite  of  the  extreme  prostration  and  ten- 
dency to  syncope  which  sometimes  attend  their  occurrence. 

When  the  recovery  from  a  bronchial  hemorrhage  is  not 
speedy,  it  is  quite  likely  to  be  followed  by  more  or  less 
febrile  excitement,  the  temperature  rising,  perhaps,  to  101° 
F.j  the  pulse  becoming  accelerated  and  feeble.  The  patient 
becomes  paler  and  weaker^  has  almost  complete  loss  of 
appetite,  is  troubled  by  a  hacking  cough  which  is  almost 
constant,  and  is  accompanied  by  a  tenacious,  scanty,  muco- 
purulent  expectoration.  The  respiration  is  hurried,  and 
there  is  dyspnoea  on  slight  exertion.  Under  these  circum- 
stances the  bronchial  hemorrhage  is  followed  by  broncho- 
pneumonia,  which,  in  the  majority  of  cases,  within  a  few 
weeks  goes  on  to  more  or  less  complete  resolution,  and  the 
patient,  by  means  of  change  of  air  and  proper  hygiene,  may 
finally  recover. 

There  is  another  class  of  cases  in  which  the  hemorrhage 
is  followed  by  still  more  active  febrile  symptoms  ;  the  tem- 
perature rises  higher,  the  pulse  is  more  rapid  and  feeble, 
emaciation  follows,  usually  accompanied  by  profuse  night- 
sweats,  and  the  patient  dies  of  acute  phthisis  within  a  few 
months  after  the  first  hemorrhage.  Previous  to  the  hemor- 
rhage he  was  in  good  health,  and  there  were  no  physical 
evidences  of  disease  of  the  lungs  or  bronchi.  This  subject 
will  be  more  fully  considered  in  connection  with  the  his- 
tory of  pulmonary  phthisis. 


112  DIFFERENTIAL  DIAGNOSIS. 

Physical  examination  of  the  chest  during  a  bronchia] 
hemorrhage  usually  gives  negative  results.  On  ausculta- 
tion nothing  abnormal  is  found,  with  the  exception  of  a 
few  large  and  small  moist  bronchial  rales.  It  is  not  well 
to  disturb  the  patient  by  frequent  examinations  of  the 
chest. 

DIFFERENTIAL  DIAGNOSIS. — There  are  four  conditions 
which  may  be  confounded  with  bronchial  hemorrhage,— 
namely,  epistaxis,  pulmonary  apoplexy,  haematemesis,  and 
aneurisms  rupturing  into  the  air-passages. 

Epistaxis  is  very  easily  distinguished  from  bronchial 
hemorrhage,  for  the  nose-bleed  occurs  before  the  apparent 
bronchial  hemorrhage,  and  the  blood  is  always  coagulated 
and  dark-colored  ;  it  is  not  attended  or  followed  by  a  cough, 
and  blood  can  always  be  detected  in  the  nostrils,  pos- 
terior nares,  or  pharynx. 

The  characteristics  of  the  haemoptysis  which  occurs  in 
connection  with  pulmonary  apoplexy,  I  have  already  suf- 
ficiently considered.  The  diagnosis  between  these  two 
forms  of  haemoptysis  rests  upon  the  character  and  quan- 
tity of  the  blood  expectorated,  and  the  existence  or  non- 
existence  of  cardiac  disease  or  pyaemia. 

Haematemesis  is  to  be  distinguished  from  bronchial  hae- 
moptysis by  the  fact  that  the  blood  in  haematemesis  is 
always  coagulated,  of  a  dark-red  color,  and  vomiting  pre- 
cedes or  accompanies  the  hemorrhage.  In  bronchial  hemor- 
rhage, if  nausea  and  vomiting  are  present,  they  follow  the 
spitting  of  arterial  blood,  and  haematemesis  is  not  accom- 
panied or  followed  by  a  cough. 

When  an  aneurism  ruptures  into  a  bronchial  tube,  gen- 
erally the  hemorrhage  is  profuse,  and  it  is  soon  followed  by 
death.  The  long  history  of  aneurism  which  precedes  the 
rupture,  as  well  as  the  physical  signs  which  at  least  will 
have  led  to  the  suspicion  of  aneurism,  in  most  instances  are 
sufficient  to  enable  one  to  determine  the  nature  of  the 
hemorrhage. 

PROGNOSIS. — The  prognosis  in  bronchial  hemorrhage  as 
regards  time  is  not  bad  ;  it  rarely  proves  immediately  fatal, 
or  directly  endangers  life. 


BEONCHIAL  HEMOEEHAGE.  113 

The  prognosis  as  to  final  result  is  always  unfavorable  ;  it 
is,  in  a  large  proportion  of  cases,  either  the  precursor  of 
phthisical  development,  or  a  sign  that  developed  phthisis 
already  exists.  It  certainly  always  demands  serious  con- 
sideration. The  prognosis  is  much  more  favorable  when 
the  hemorrhage  is  due  to  excessive  action  of  the  heart,  or 
bronchial  hypersemia  induced  by  the  inhalation  of  irritating 
substances  or  gases,  than  when  it  occurs  without  any  appa- 
rent exciting  cause. 

TEEATMENT. — The  most  important  element  in  the  treat- 
ment of  bronchial  hemorrhage,  is  absolute  rest  in  a  cool 
room.  The  patient  should  be  placed  in  bed  and  not  allowed 
to  sit  up,  turn  over,  or  even  speak  above  a  whisper.  If 
the  cough  continues  and  is  constant,  or  induces  the  hemor- 
rhage, it  must  be  quieted  by  full  doses  of  opium.  Ergot, 
spirits  of  turpentine,  persulphate  of  iron,  or  common  salt 
may  be  administered,  if  their  administration  will  quiet  the 
anxiety  of  the  patient  or  friends.  It  has  never  seemed  to 
me  that  styptics  or  astringents  have  any  control  over  bron- 
chial hemorrhages.  The  application  of  ice-bags  to  the  sur- 
face of  the  chest  may  be  resorted  to  in  extreme  cases,  but 
it  must  be  carefully  done,  for  the  reason  that  patients  to 
whom  ice-bags  are  applied  are  exceedingly  liable  to  have 
broncho-pneumonia  follow  their  attacks  of  bronchial  hem- 
orrhage. 

Dry-cupping  over  the  surface  of  the  chest  is  of  service 
whenever  the  hemorrhage  is  preceded  or  attended  by  marked 
pulmonary  hypersemia. 

Patients  with  haemoptysis  should  be  urged  to  eat  ice  and 
drink  freely  of  cold  drinks. 

In  all  cases  of  bronchial  hemorrhage  it  is  important  to 
keep  the  patient  under  observation  until  all  bronchial  irri- 
tation produced  by  the  presence  of  blood  in  the  bronchial 
tubes  has  subsided.  If  there  is  tendency  to  a  return  of  the 
hemorrhage,  everything  likely  to  bring  on  an  attack  must 
be  carefully  avoided,  and  you  must  endeavor  to  improve 
the  nutrition  of  the  patient,  by  the  administration  of  iron 
combined  with  a  most  nutritious  but  non-stimulating  diet. 
Moderate  exercise  should  be  taken  daily  in  the  open  air, 


114  MOKBID   ANATOMY. 

and  all  mental  and  physical  excitement  should  be  carefully 
avoided.  I  will  now  briefly  speak  of  gangrene  and  cancer 
of  the  lungs,  although  they  have  no  necessary  connection 
with  bronchial  hemorrhage. 

GANGRENE  OP  THE  LUNGS. 

There  are  two  recognized  forms  of  pulmonary  gangrene ; 
namely,  the  circumscribed  and  the  diffused. 

Circumscribed  gangrene  of  the  lungs  is  of  much  more  fre- 
quent occurrence  than  the  diffused  variety. 

MORBID  ANATOMY. — In  circumscribed  pulmonary  gan- 
grene, small  isolated  portions  of  lung-tissue  become  converted 
into  bluish-green  fetid  sloughs,  which  at  first  are  firm  and  sur- 
rounded by  oadematous  lung- tissue,  but  they  soon  decompose 
into  an  ichorous  fluid,  which  may  be  discharged  through  a 
bronchus  and  leave  a  ragged  sloughy  cavity,  surrounded  by 
inflamed  lung-tissue.  Vessels  may  traverse  this  cavity,  but 
as  coagula  rapidly  form  in  them,  hemorrhage  rarely  occurs. 

Sometimes,  by  the  gangrenous  process  an  opening  is 
formed  into  the  pleural  cavity  which  causes  acute  pleurisy, 
or  hydro-pneumothorax.  The  gangrenous  cavity  may  open 
into  a  bronchial  tube ;  sometimes  a  spot  of  circumscribed 
gangrene  becomes  the  centre  of  diffused  gangrene.  In  ex- 
ceptional cases,  the  disorganized  portion  is  expelled,  a 
fibrous  capsule  forms,  and  healthy  pus  is  produced.  In  such 
cases  the  cavity  may  ultimately  close  up  and  cicatrize. 

The  seat  of  circumscribed  pulmonary  gangrene  is  usually 
in  the  lower  lobes  or  on  the  surface  of  the  lungs. 

In  diffused  gangrene  of  the  lung,  not  unfrequently  an 
entire  lobe  is  involved,  and  sometimes  an  entire  lung  ;  unlike 
the  preceding  form,  there  is  no  line  of  demarcation  ;  the  gan- 
grenous processes  are  not  abruptly  limited,  but  gradually 
merge  into  redematous  or  hepatized  lung-tissue. 

The  affected  pulmonary  tissue  is  more  or  less  decomposed 
and  converted  into  a  putrid  mass,  which  is  saturated  with  a 
grayish-black  fluid ;  as  the  gangrenous  process  reaches  the 
pleura,  it  becomes  destroyed.  Recovery  under  these  cir- 
cumstances rarely,  if  ever,  takes  place,  the  patient  dying 
of  septicremia  or  pya3inia. 


GA1STGEENE   OF   THE  LUNGS.  115 

ETIOLOGY. — The  conditions  under  which  gangrene  of  lung- 
tissue  may  occur  are  numerous,  and  need  little  more  than 
their  enumeration  for  you  to  appreciate  their  mode  of  oper- 
ation. 

First. — Gangrene  of  the  lungs  may  occur  as  the  result  of 
certain  local  pulmonary  diseases,  such  as  acute  or  chronic 
pneumonia,  cancer,  hydatids,  bronchial  dilatation,  hemor- 
rhagic  infarctions  from  embolism,  obstruction  in  the  nutrient 
vessels  leading  to  the  gangrenous  portions. 

Second. — Pulmonary  gangrene  may  occur  in  connection 
with  blood-poisoning,  such  as  is  met  with  in  low  fevers, 
pyaemia,  septicaemia,  glanders,  etc. 

Third. — Gangrene  of  the  lungs  sometimes  occurs  in  cer- 
tain nervous  diseases,  as  dementia,  softening  of  the  brain, 
epilepsy,  and  chronic  alcoholismus.  It  is  difficult  to  explain 
the  occurrence  of  diffused  pulmonary  gangrene  in  lunatics 
and  drunkards. 

SYMPTOMS. — The  symptoms  of  this  affection,  at  its  com- 
mencement, are  often  very  obscure.  When  it  develops  from 
hemorrhagic  infarction,  its  presence  cannot  generally  be 
diagnosticated  until  the  gangrenous  process  reaches  a  bron- 
chial tube  of  considerable  size. 

The  two  symptoms  which  most  positively  indicate  the 
existence  of  pulmonary  gangrene,  are  an  extremely  fetid 
breath,  and  the  expectoration  of  gangrenous  material ;  some- 
times the  fetid  breath  precedes  the  characteristic  expectora- 
tion. The  color  of  the  expectoration  is  usually  a  dirty  black 
or  brown,  which  contains  small  black  masses,  and  in  rare 
instances  the  wavy  elastic  fibres  of  lung-tissue  are  to  be 
found  in  it ;  more  or  less  blood  is  often  present,  and  death 
may  occur  from  hemorrhage. 

In  some  cases  there  is  but  slight  constitutional  disturb- 
ance, and  the  gangrenous  process  goes  on  for  weeks  before 
there  are  any  general  symptoms  to  indicate  its  presence. 
In  other  cases,  from  the  beginning  the  greatest  prostration 
is  experienced,  the  pulse  becomes  small  and  frequent,  and 
the  vital  powers  rapidly  give  way  before  the  septic  fever. 
Occasionally,  death  takes  place  from  the  exhaustion  result- 
ing from  slow,  hectic  fever. 


116  DIFFERENTIAL  DIAGNOSIS. 

When  diffuse  gangrene  of  the  lung  occurs  in  connection 
with  pneumonia,  its  occurrence  is  marked  by  a  sudden 
prostration,  accompanied  by  a  small,  irregular  pulse,  a  dis- 
turbed, anxious  countenance,  a  fetid  breath,  and  a  black, 
liquid  expectoration  having  a  gangrenous  odor.  If  the  gan- 
grenous material  is  swallowed,  as  sometimes  happens,  severe 
diarrhoaa  and  tympanitic  distention  of  the  abdomen  occur. 

PHYSICAL  SIGNS. — The  physical  signs  of  pulmonary  gan- 
grene are  often  obscure,  and  never  distinctive.  They  are 
those  of  local  consolidation  followed  by  the  evidences  of 
breaking  up  of  lung-tissue,  and  the  formation  of  cavities 
in  the  lung-substance.  There  are  no  special  signs  indicating 
the  nature  of  the  disorganizing  process ;  sometimes  it  is 
preceded  by  the  signs  of  pneumonia,  generally  it  is  accom- 
panied by  signs  of  bronchitis,  and  in  the  later  stages  of  the 
disease  there  are  physical  evidences  of  the  formation  of 
cavities  in  the  lung-substance. 

DIFFERENTIAL  DIAGNOSIS. — The  diagnosis  of  gangrene  of 
the  lungs  rests  almost  entirely  on  the  characteristic  odor 
and  appearance  of  the  expectoration  ;  prior  to  its  occur- 
rence the  existence  of  gangrene  cannot  be  determined. 
Gangrenous  expectoration,  accompanied  by  the  physical 
evidences  of  softening  and  excavation  of  pulmonary  sub- 
stance, is  sufficient  for  its  diagnosis. 

There  may  arise  certain  conditions  in  which  it  will  be 
difficult  to  make  a  differential  diagnosis ;  as,  for  example, 
in  some  cases  of  fetid  bronchitis  there  may  be  a  profuse,, 
greenish,  sero-purulent  expectoration,  attended  by  an  ex- 
tremely fetid  odor,  not  distinguishable  from  that  of  gan- 
grene, and  yet  no  true  gangrene  of  the  lung  exists. 

Again,  gangrene  of  the  lung  may  exist  without  any  per- 
ceptible fetor  in  the  breath,  or  expectoration,  or  any  of  the 
other  attendant  symptoms  of  gangrene.  Under  such  cir- 
cumstances the  gangrenous  portion  of  the  lung  does  not 
communicate  with  a  bronchial  tube. 

Again,  local  gangrene  may  occur  in  a  phthisical  cavity ; 
when  it  does,  it  is  very  difficult  to  distinguish  it  from  true 
gangrene  of  the  lung,  especially  if  the  patient  is  seen  for  the 
first  time  just  as  the  gangrenous  process  is  established. 


GANGRENE  OF  THE  LUNGS.  117 

A  fetid  abscess  is  generally  distinguished  from  true  pul 
monary  gangrene,  not  by  the  character  of  the  fetor,  but  by 
the  fact  that  the  signs  of  excavation  precede  the  occurrence 
of  the  fetor,  while  in  true  gangrene  of  the  lung  the  signs  of 
excavation  follow  the  gangrenous  expectoration. 

In  all  cases,  in  order  to  make  a  correct  diagnosis,  it  is 
necessary  that  you  have,  in  addition  to  the  fetid  breath  and 
expectoration,  decomposed  pulmonary  tissue  in  the  ex- 
pectorated matter. 

PROGNOSIS. — The  prognosis  is  always  unfavorable,  al- 
though the  disease  may  not  be  regarded  as  absolutely  fatal. 
Recovery  can  only  take  place  in  those  cases  where  the  gan- 
grene is  circumscribed,  and  limited  to  a  small  portion  of 
lung-tissue ;  under  such  circumstances  it  is  possible  for  the 
slough  to  separate,  be  discharged,  and  induration  and  final 
cicatrization  of  lung-tissue  to  take  place. 

Diffused  pulmonary  gangrene  is  always  fatal.  Sometimes 
death  is  the  result  of  profuse  hemorrhage  ;  at  other  times  it 
is  due  to  perforation,  of  the  pleura ;  but  more  frequently 
the  patient  dies  from  the  exhaustion  which  attends  the 
septic  poisoning. 

TREATMENT. — Under  no  circumstances  are  you  justified 
in  resorting  to  depressing  remedies ;  on  the  contrary,  in 
every  possible  way  you  must  sustain  the  vital  powers  of 
your  patient  by  the  administration  of  stimulants,  tonics, 
and  a  most  nutritious  diet.  Opium  may  be  given  in  moder- 
ate doses  to  alleviate  pain,  allay  cough,  and  overcome  con- 
stitutional irritation. 

I  have  never  found  antiseptic  inhalations  to  produce  the 
beneficial  effects  claimed  for  them  by  some  authorities,  nor 
have  I  been  able,  by  the  internal  administration  of  chlorate 
of  potash,  to  obtain  any  satisfactory  results. 

My  own  experience  leads  me  to  believe  that  all  this  class 
of  remedies  can  neither  arrest  the  gangrenous  process,  nor 
even  mitigate  its  unpleasant  eifects. 

CANCER  OF  THE  LUNGS. 

This  disease  is  exceedingly  rare,  and  is  usually  secondary 
to  cancerous  developments  in  other  parts  of  the  body. 


118  MOEBID   ANATOMY. 

MOEBID  ANATOMY. — The  medullary  variety  of  cancer  is 
almost  the  only  variety  met  with  in  the  lungs,  although 
epithelial  and  melanotic  cancer  of  the  lungs  are  spoken  of 
by  most  authorities. 

Medullary  cancer  of  the  lungs  occurs  in  the  form  of 
nodules  of  various  sizes,  scattered  through  the  lung-sub- 
stances, or  a  large  portion  of  lung  may  become  the  seat  of 
medullary  infiltration. 

Primary  cancer  usually  involves  only  one  lung,  and  is 
often  infiltrated,  while  secondary  cancer  affects  both  lungs, 
and  is  generally  nodular,  the  nodules  varying  in  size.  By 
the  union  of  the  nodules,  sometimes  an  entire  lung  becomes 
involved.  After  a  time,  the  cancerous  matter  undergoes 
fatty  degeneration  and  softening ;  the  pulmonary  vessels 
and  bronchi  are  either  involved  in  the  cancerous  develop- 
ment, or  are  obliterated  by  its  pressure.  The  unaffected 
portion  of  lung-tissue  may  be  normal,  oedematous,  or  pneu- 
monic ;  extensive  pleuritic  thickenings  and  adhesions  are 
present  in  most  cases. 

ETIOLOGY. — The  question  of  the  etiology  of  cancer  of  the 
lung  involves  the  etiology  of  cancer  in  general,  and  is  as 
obscure  as  the  origin  of  other  malignant  neoplasms. 

Hereditary  predisposition  must  always  be  regarded  as  an 
important  element  in  its  production.  It  is  most  frequently 
met  with  between  the  ages  of  forty  and  sixty,  and  is  more 
common  in  males  than  in  females.  As  has  already  been 
stated  it  is  generally  secondary  to  cancerous  developments  in 
other  organs  of  the  body.  In  the  female,  cancer  of  the  breast 
usually  precedes  the  development  of  cancer  of  the  lungs. 

SYMPTOMS. — Cancer  of  the  lungs  usually  comes  on  very 
insidiously,  with  few  subjective  symptoms.  There  is  usually 
some  pain  in  the  chest,  and  a  cough  accompanied  by  an 
expectoration  resembling  currant-jelly,  occasionally  con- 
taining cancerous  elements.  Usually  more  or  less  dyspnoea 
is  present,  especially  if  there  exists  at  the  same  time  medi- 
astinal  tumors.  The  cancerous  cachexia  may  or  may  not 
be  present.  As  the  disease  advances,  emaciation,  fever, 
night-sweats,  with  failure  of  strength,  become  more  and 
more  marked. 


CANCER  OF  THE  LUNGS.  119 

If  dyspnoea,  cough,  haemoptysis,  pain  in  the  chest,  and 
rapid  emaciation  with  cancerous  cachexia  should  come  on 
in  one  from  whom  a  carcinomatous  breast  had  been  extir- 
pated, you  would  have  reason  to  suspect  the  development 
of  cancer  of  the  lung. 

PHYSICAL  SIGNS. — These  will  vary  according  to  the  seat 
and  amount  of  the  cancerous  accumulation. 

If  the  lung  is  extensively  involved  with  nodular  cancer, 
inspection  will  show  enlargement  of  the  affected  side,  with 
widening  of  the  intercostal  spaces,  and  deficience  or  entire 
absence  of  respiratory  movement.  Palpation  will  give 
diminished,  or  absence  of,  vocal  fremitus.  On  percussion, 
there  will  be  complete  dulness  unattended  by  friction  over 
the  space  corresponding  to  the  cancerous  walls. 

On  auscultation,  the  respiratory  sounds  may  be  feeble  or 
absent,  or  if  a  large  open  bronchus  is  intimately  connected 
with  the  cancerous  mass,  bronchial  respiration  may  be 
heard. 

Disseminated  cancer  of  the  lungs  cannot  be  distinguished 
by  physical  examination  from  simple  bronchial  catarrh. 

In  the  infiltrated  form  the  lung  is  often  contracted,  and  as 
a  consequence,  there  is  retraction  of  the  chest- walls  over  the 
affected  lung. 

DIFFERENTIAL  DIAGNOSIS. — The  only  disease  with  which 
pulmonary  cancer  is  liable  to  be  confounded  is  pleurisy 
with  serous  effusion.  In  cancer,  however,  the  percussion 
dulness  does  not  begin  at  the  bottom  of  the  chest,  while  in 
pleurisy  it  does ;  in  cancer,  the  dulness  is  most  marked  in 
front,  whereas  in  pleurisy  it  is  most  marked  behind ;  in 
cancer,  you  will  be  able  to  detect  one  or  more  isolated  spots 
of  resonance  in  the  dull  space,  while  in  pleurisy  the  dul- 
ness is  over  all  the  space  occupied  by  the  fluid. 

PROGNOSIS. — This  disease  is  necessarily  fatal,  death  occur- 
ring either  from  local  or  general  causes. 

TREATMENT. — This  is  altogether  palliative,  as  it  is  restrict- 
ed to  the  relief  of  symptoms. 


LECTURE  X. 


PNEUMONIA. 

i 

Varieties. — Croupous  or  Lobar  Pneumonia. 

WE  will  now  commence  the  history  of  a  very  common, 
and,  at  the  same  time,  a  very  important  form  of  disease. 
Some  diseases  are  of  interest  on  account  of  the  rarity  of 
their  occurrence,  but  the  one  which  is  now  to  engage  our 
attention  is  of  interest  on  account  of  its  frequency.  You 
will  be  sure  to  meet  with  it  very  soon  after  you  enter  on  the 
active  duties  of  your  profession,  and  the  dangers  which 
attend  its  development  will  always  cause  you  more  or  less 
anxiety. 

Strictly  speaking,  pneumonia  is  an  inflammation  of  the 
vesicular  structure  of  the  lungs.  When  it  affects  the  alveoli, 
they  become  filled  with  inflammatory  exudation  ;  when  the 
interstitial  tissue  is  involved  it  becomes  increased  in  amount. 
The  inflammation  may  extend  to  the  bronchi  and  to  the 
pleura,  so  that  in  one  sense  pneumonia  may  be  regarded  as 
an  affection  of  the  whole  lung. 

Clinically,  as  well  as  pathologically,  there  are  three  dis- 
tinct types  of  pneumonia,  each  of  which  requires  a  separate 
consideration. 

First. — CROUPOUS  or  LOBAR  PNEUMONIA,  which  is  always 
acute. 

Second. — CATARRHAL  or  LOBULAR  PNEUMONIA,  sometimes 
designated  BROXCHO-PNEUMONIA,  which  may  be  acute  or 
chronic. 


PNEUMONIA.  121 

Third. — INTERSTITIAL  PNEUMONIA,  or  fibrous  induration 
of  the  lung. 

CROUPOUS  OR  LOBAR  PNEUMONIA. 

This  is  one  of  the  most  common  acute  diseases  of  adult 
life.  When  the  unqualified  term  pneumonia  is  used, 
this  variety  is  referred  to.  It  usually  involves  the  whole 
of  the  affected  lobe,  and  on  this  account  has  been  called 
lob ar  pneumonia  ;  it  may  extend  over  the  whole  of  one  or 
both  lungs.  Some  have  given  to  this  form  of  pneumonia 
the  term  pleuro-pneumonia,  for  the  reason  that  when  the 
surface  of  the  lung  is  involved,  the  pleura  which  covers 
that  portion  is  also  inflamed,  but  the  pleurisy  is  secondary 
to  the  pneumonia.  When  the  pleurisy  is  the  primary  affec- 
tion, then,  properly  speaking,  the  disease  is  a  pleuro-pneu- 
monia.  It  is  important  to  recognize  the  two  conditions, 
and  distinguish  them  from  each  other. 

MORBID  ANATOMY. — Anatomically,  as  well  as  clinically, 
croupous  pneumonia  may  be  divided  into  three  stages  : 

First. — A   STAGE   OF   CONGESTION    OE  ENGOKGEMENT. 

Second. — A  STAGE  OF  BED  HEPATIZATION  OR  CONSOLI 

DATION. 

Third. — A  STAGE  OF  GRAY  HEPATIZATION  AND  RESOLU- 
TION,— sometimes  of  purulent  infiltration. 

I  shall  describe  separately  the  morbid  anatomy  of  these 
different  stages. 

In  the  first  stage,  or  stage  of  engorgement,  that  portion 
of  the  lung  which  is  involved  in  the  pneumonic  process 
does  not  collapse  when  the  thoracic  cavity  is  opened  ;  the 
affected  portion  of  lung  is  distended,  and  is  firmer  than 
natural ;  it  is  of  a  dark  red  color,  is  heavier,  and  crepitates 
less  than  normal  lung-tissue.  On  section,  a  reddish  fluid 
escapes  from  the  air-cells,  which  is  coagulated  by  alcohol 
into  an  amorphous,  granular  substance,  and  dark  blood 
flows  from  the  distended  capillaries  around  the  air-cells. 
On  microscopical  examination  of  a  portion  of  the  affected 
lung-tissue,  the  blood-vessels  of  the  alveoli  will  be  found 
distended  with  blood  and  projecting  into  the  cavity  of  the 
air-cells,  which,  with  the  eifusion,  diminish  their  calibre. 


122  MOEBID   ANATOMY. 

Anatomically,  this  condition  differs  from  simple  pulmo- 
nary congestion  and  oedema,  in  the  character  of  the  fluid 
which  is  found  in  the  air-cells,  and  in  the  change  in  the 
capillary  vessels  ;  in  cedema,  the  fluid  in  the  air-cells  is 
simply  serum, — in  pneumonia  it  is  an  inflammatory  exuda- 
tion. It  also  differs  from  brown  induration  in  the  character 
of  the  cell-contents, — in  brown  induration  the  alveoli  con- 
tain cells  which  have  become  pigmented.  All  forms  of 
pulmonary  congestion  somewhat  resemble  the  first  stage  of 
pneumonia  ;  the  most  reliable  distinction  is  to  be  found  in 
the  difference  in  the  contents  of  the  cavity  of  the  alveoli. 

In  the  second  stage,  or  stage  of  red  Jiepatization,  the 
affected  portion  of  lung  becomes  solid,  heavy,  and  airless  ; 
a  portion,  when  thrown  into  w^ater,  quickly  sinks  to  the 
bottom  of  the  vessel.  It  is  of  a  dark-red  or  brownish  color  ; 
in  its  general  appearance  it  resembles  normal  liver-tissue, 
hence  the  name  red  hepatization.  On  section,  the  cut  sur- 
face has  a  granular  appearance.  The  granules  are  more 
distinct  on  the  torn  than  on  the  cut  surface  ;  each  granule  can 
be  lifted  out  of  the  lung-substance  with  a  needle,  and  it 
corresponds  in  size  to,  and  constitutes  the  contents  of,  an 
air-cell.  If  the  examination  is  made  soon  after  death,  the 
cut  or  torn  surface  is  dry  ;  if  it  is  delayed  twelve  or  four- 
teen hours,  the  surface  will  be  covered  with  a  thick,  grumous, 
reddish-gray  fluid,  the  result  of  post-mortem  changes. 

Not  unfrequently  the  smaller  bronchi  are  filled  with  a 
firm,  yellow,  fibrinous  material;  it  is  of  the  same  kind  as 
that  which  fills  the  air-cells. 

On  firm  pressure  with  the  finger,  the  consolidated  lung- 
tissue  is  readily  broken  down. 

On  microscopical  examination,  the  alveoli  and  smaller 
bronchi  are  found  filled  with  a  solid  exudation.  This  ex- 
udation consists  of  fibrillated  fibrin,  enclosing  in  its  meshes 
a  variable  number  of  red  blood-globules  and  cells.  These 
sells  have  been  denominated  pus-cells,  pneumonic  globules, 
exudation  corpuscles,  and  white  blood-globules  or  lymphoid 
cells,  according  to  the  different  views  entertained  by  dif- 
ferent observers  in  regard  to  their  origin.  Undoubtedly, 
the  white  globules,  or  lymphoid  cells,  are  the  most  nu- 


PNEUMONIA.  123 

merous.  The  large  polygonal  nucleated  cells  are  changed 
epithelium. 

All  of  these  different  cells,  at  times,  have  been  regarded 
as  characteristic  of  pneumonia.  The  red  globules  give  the 
color  to  the  consolidated  lung. 

The  number  of  cells  present  will  vary  very  much  in  dif- 
ferent pneumonias  ;  the  fibrin  also  varies  in  quantity,  but 
some  fibrillated  fibrin  is  always  present  in  the  second  stage 
of  this  variety  of  pneumonia. 

The  walls  of  the  alveoli  are  unchanged,  and  the  capillary 
plexus  in  their  walls  contains  less  blood  than  in  the  first 
stage. 

In  the  tliird  stage,  or  stage  of  gray  Jiepatization,  the 
consolidated  lung  is  changed  in  color ;  it  is  no  longer  deep 
red  or  brown,  but  of  a  gray  color ;  at  first,  its  consistency 
and  gross  appearance  remain  unchanged.  The  change  in 
color  is  gradual ;  at  first  the  consolidation  presents  a 
mottled  appearance,  red  and  gray ;  afterwards  it  becomes 
entirely  gray.  This  change  in  color  is  due  to  a  decolora- 
tion of  the  red  globules  which  were  effused  into  the  cavity 
of  the  air-cells  during  the  second  stage.  As  the  consolida- 
tion becomes  more  and  more  gray  in  color,  there  is  a  steady 
increase  in  the  number  of  lymphoid  cells  in  the  cavity  of  the 
alveoli,  and  they  gradually  become  distended  with  shining- 
granules. 

With  the  change  in  color,  usually  the  firmness  of  the  ex- 
udation in  the  alveoli  is  diminished,  until,  finally,  they  are 
filled  with  a  fluid  mass,  which  is  easily  removed  ;  sometimes 
a  change  in  color  is  not  accompanied  by  a  change  in  the 
elements  of  the  exudation. 

When  resolution  follows  a  change  in  the  color  of  the  con- 
solidation, the  fibrin  in  the  alveoli  and  small  bronchi  be- 
comes granular,  the  red  globules  disappear,  the  cells  undergo 
fatty  degeneration,  and  a  serous  fluid  exudes  from  the 
blood-vessels,  transposing  the  whole  into  a  dirty  white 
emulsion  ;  a  part  of  this  product  is  removed  by  expectora- 
tion, and  a  part  (sometimes  the  whole)  by  absorption. 

During  this  stage  the  lung  remains  greenish  or  yellowish ; 
gradually  it  becomes  less  granular,  lighter,  and  moist,  and, 


124  MOBBID   ANATOMY. 

when  pressed  upon,  readily  exudes  fluid  from  its  cut  sur- 
face. 

Its  elasticity  remains  impaired  not  only  during,  but  long 
after  this  stage,  its  vessels  are  more  congested,  and  its  tissue 
darker. 

As  the  resolution  is  completed,  the  epithelial  lining  of  the 
air-cells,  which  has  been  destroyed  during  the  progress  of 
the  inflammatory  process,  is  restored  ;  the  blood  returns  to 
its  normal  channels,  and  the  lung  is  restored  to  its  normal 
condition,  and  thus  (when  the  disease  runs  an  uncompli- 
cated course)  complete  restoration,  both  structural  and 
functional,  takes  place  in  that  portion  of  lung- tissue  which 
has  been  the  seat  of  the  pneumonia. 

While  the  exudation  into  the  air-cells  is  taking  place,  the 
smaller,  and  sometimes,  though  rarely,  the  larger  bronchi 
become  filled  with  cylindrical  or  tubular  croupous  products  ; 
this  exudation  is  of  the  same  character  as  that  which  fills 
the  cavities  of  the  alveoli,  and  after  undergoing  similar 
changes  is  removed  by  expectoration  and  absorption. 

The  pleura  over  the  inflamed  lung  is  congested,  opaque, 
ecchymotic,  and  coated  with  lymph,  while  rarely  fluid  is 
found  in  the  pleural  sac  ;  while  resolution  of  the  pneumonia 
is  taking  place,  the  exudation  which  has  occurred  on  the 
surface  of  the  pleura  may  remain,  and  sufficient  thickening 
of  the  pleura  may  take  place,  to  give  rise  to  some  dulness 
on  percussion ;  the  dull  percussion,  which  often  remains 
after  convalescence  is  established  in  a  case  of  pneumonia,  is 
due  partly  to  pleuritic  changes,  and  partly  to  the  distended 
condition  of  the  pulmonary  capillaries. 

Purulent  infiltration  sometimes  takes  place  in  the  third 
stage  of  pneumonia ;  in  such  cases  the  rapid  production  of 
cells  is  a  marked  lesion  during  the  stage  of  gray  hepatiza- 
tion.  These  cells  have  all  the  characteristics  of  pus-cells, 
and  are  cells  which  have  a  constitution  identical  with  the 
white  blood-globules ;  they  increase  the  distention  of  the 
alveoli  and  are  intimately  mixed  with  the  other  inflamma- 
tory products.  Why  in  certain  conditions  in  gray  hepati- 
zation  this  process  of  rapid  cell  formation  occurs,  is  not 
easily  explained. 


PNEUMONIA.  125 

When  purulent  infiltration  occurs,  the  portion  of  lung 
affected  assumes  a  more  yellow  color,  is  more  friable  and 
moist ;  the  cells  are  found  in  the  alveoli  and  between  the 
vesicles ;  gradually,  however,  they  cease  to  be  produced, 
undergo  fatty  degeneration,  are  absorbed  or  expectorated, 
and  the  lung  returns  to  its  normal  state,  or  the  patient  sinks 
and  dies  of  exhaustion.  If  an  cedematous  condition  of  the 
intervesicular  structure  occurs,  as  happens  in  certain  con- 
ditions of  the  system,  resolution  is  impossible ;  all  the  tis- 
sues of  the  lung  become  infiltrated  with  pus-cells,  break 
down  and  form  abscesses ;  these  abscesses  may  be  single  or 
multiple.  The  cavities  of  these  abscesses  will  contain 
broken-down  lung-tissue  and  pus.  These  may  increase  by 
peripheral  growth,  or  by  the  running  together  of  adjacent 
abscesses,  so  as  to  occupy  a  greater  portion  of  a  lobe ;  at 
first  their  walls  are  yellow,  and  infiltrated  with  pus. 

In  whatever  way  these  abscesses  are  formed,  they  usually 
lead  to  death,  although  there  is  a  chance  of  recovery  when 
they  open  into  a  bronchus  of  sufficient  size  to  permit  a  free 
discharge  of  their  contents.  Under  such  circumstances  the 
contents  of  the  abscess  is  expectorated,  interstitial  inflam- 
mation is  set  up  around  it,  and  at  length  it  becomes 
enclosed  by  firm  walls,  contraction  ensues,  and  finally 
nothing  but  cicatricial  tissue  marks  its  former  situation. 
Again  there  is  a  chance  of  recovery,  if  no  bronchial  com- 
munication is  established,  when  the  abscess  becomes  encap- 
sulated by  firm,  callous  tissue  ;  then  its  contents  degenerate 
into  a  cheesy  mass  and  afterwards  becomes  calcareous. 
The  smaller  the  abscess  the  more  likely  is  it  to  reach  this 
termination.  Sometimes  these  abscesses  reach  the  sur- 
face of  the  lung,  perforate  the  pleura,  and  discharge  their 
contents  into  the  pleural  cavity,  causing  hydro-pneumo- 
thorax. 

From  an  anatomical  point  of  view,  the  terminations  of 
this  form  of  pneumonia  are  resolution,  gangrene,  and 
ibscess.  Death  may  occur  in  any  stage  of  the  disease  ;  it 
most  frequently  occurs  in  the  second  and  third  ;  not 
(infrequently  it  is  produced  by  congestion  and  oedema  of 
the  sound  portion  of  the  lung. 


126  ETIOLOGY. 

If  gangrene  occurs,  it  may  be  diffused  or  circumscribed, 
and  depends  either  upon  arterial  emboli  or  venous  thrombi. 

It  is  claimed  by  some  that  the  products  of  this  variety  of 
pneumonia  in  part  or  throughout  the  inflamed  portion  may 
become  cheesy,  and  thus  constitute  one  form  of  phthisis. 
This  is  not  a  frequent  termination,  and  when  it  occurs,  a 
more  than  usually  abundant  cell-formation  takes  place, 
either  in  the  second  or  third  stage  of  the  disease,  after  which 
a  drying  down  of  the  contents  of  the  alveoli  takes  place  ; 
it  may  occur  in  previously  healthy  persons,  but  it  is  more 
likely  to  occur  in  the  debilitated. 

When  croupous  pneumonia  runs  a  more  chronic  course 
than  ordinarily,  the  interstitial  tissue  becomes  involved, 
increased  development  of  fibrous  tissue  is  the  consequence, 
and  we  have  an  interstitial  pneumonia  developed.  I  shall 
consider  this  more  fully  under  the  head  of  pulmonary 
phthisis. 

ETIOLOGY. — Among  the  predisposing  causes  of  croupous 
pneumonia,  age  stands  first.  You  will  rarely  meet  with  it 
in  children  under  five  years  of  age,  and  most  frequently 
meet  with  it  in  persons  between  twenty  and  forty,  and 
more  than  sixty  years  of  age.  It  is  comparatively  rare 
between  the  ages  of  forty  and  sixty,  although  no  age  is 
exempt.  It  occurs  more  frequently  in  males  than  in 
females.  Poverty,  intemperance,  and  occupations  requir- 
ing exposure  to  sudden  changes  of  temperature,  predispose 
to  pneumonia. 

It  occurs  more  frequently  in  climates  subject  to  sudden 
variations  of  temperature,  than  in  those  which  maintain  a 
continuous  high  or  continuous  low  temperature,  hence 
pneumonia  is  rarely  met  with  in  the  tropics,  or  in  the  cold 
regions  of  the  north  ;  westerly  and  easterly  winds  greatly 
predispose  to  its  occurrence.  We  meet  with  it  among  those 
who  are  weak  and  feeble,  rather  than  strong  and  vigorous. 
Persons  convalescing,  from  any  grave  form  of  disease  are 
especially  liable  to  an  attack  of  pneumonia.  Previous  at- 
tacks increase  the  liability  to  its  occurrence. 

The  exciting  causes  are  often  obscure  ;  but  there  are 
many  cases  of  primary  pneumonia  which  unquestionably 


PKEFMONIA.  127 

arise  from  a  sudden  chill  when  the  body  is  heated,  the  result 
of  exposure  to  cold  and  wet,  or  to  a  draught. 

Unknown  atmospheric  conditions  undoubtedly  act  as  ex- 
citing causes ;  this  is  especially  noticeable  in  connection  with 
such  atmospheric  conditions  as  give  prevalence  to  other  in- 
flammatory diseases.  What  the  element  is  which  is  pres- 
ent in  the  atmosphere  and  produces  such  results,  has  not 
yet  been  determined  ;  epidemic  pneumonia  has  such  an  ex- 
citing cause.  Not  unfrequently  it  is  excited  by  the  specific 
poisons  of  various  acute  affections,  as  the  essential  exan- 
thematous  and  malarial  fevers. 

All  that  class  of  diseases  which  depend  upon  the  retention 
in  the  body  of  some  morbid  product,  as  pyaemia,  septi- 
caemia, ursemia,  etc.,  are  especially  liable  to  be  complicated 
with  it. 

It  is  also  of  very  frequent  occurrence  in  chronic  blood 
diseases,  such  as  chronic  alcoholismus. 

The  extension  of  inflammation  from  tissues  adjacent  to 
the  lungs,  to  the  lungs  themselves,  is  also  an  exciting  cause. 
This  is  shown  in  pleuro-pneumonia, — it  may  be  developed 
in  connection  with  pericarditis,  or  from  the  extension  of  an 
inflammation  from  the  abdominal  organs. 

The  traumatic  causes  which  may  give  rise  to  it  are  almost 
innumerable. 

Opinions  differ  in  regard  to  the  production  of  pneumonia 
by  the  inhalation  of  cold  air. 

Intense  or  long-continued  pulmonary  congestion  is  very 
liable  to  cause  it ;  especially  when  it  occurs  in  connection 
with  heart  disease,  or  hypostatic  congestion. 

From  the  recital  of  the  exciting  causes  of  this  disease,  it  is 
evident  that  its  occurrence  as  a  primary  affection  is  com- 
paratively rare  ;  almost  all  cases  can  be  traced  to  some  well- 
recognized  exciting  cause.  As  I  have  already  stated,  in  the 
majority  of  cases  pneumonia  occurs  when  the  patient  is  in 
a  debilitated  condition. 

A  man  may  be  saturated  in  alcohol,  every  organ  in  his 
body  may  be  under  its  influence :  he  sits  in  a  draught,  or 
in  some  way  his  surface  becomes  chilled,  a  pneumonia  fol- 
lows, but  that  pneumonia  is  not  idiopathic. 


128  SYMPTOMS. 

Again,  a  man  may  be  ursemic,  or  charged  with  malaria, 
and  from  a  slight  exposure  he  develops  a  pneumonia,  but  it 
is  not  of  idiopathic  origin. 

This  view  of  its  causation  will  have  an  important  bearing 
upon  the  question  of  treatment,  when  we  reach  that  part  of 
its  history. 

I  believe  an  idiopathic  pneumonia  is  of  very  rare  occur- 
rence. 

SYMPTOMS. — In  the  majority  of  cases,  the  invasion  of 
croupous  pneumonia  is  sudden ;  it  is  ushered  in  by  a  distinct 
chill,  which  lasts  from  half  an  hour  to  two  or  three  hours  ; 
the  intensity  and  constancy  of  the  chill  is  greater  than  in 
any  other  disease  except  malarial  fever,  pyaemia,  and  puer- 
peral fever.  Usually  the  chill  may  be  distinguished  from 
the  chills  of  other  diseases  by  its  violence  and  short  dura- 
tion. If  the  chill  is  absent,  its  invasion  may  be  marked  by 
great  prostration,  and  symptoms  of  collapse.  In  children, 
convulsions,  vomiting,  headache,  and  delirium  may  mark 
the  period  of  its  invasion.  In  old  people,  after  the  age  of 
seventy,  the  chill  is  frequently  absent.  This  fact  should  be 
remembered,  as  in  very  many  cases  among  old  people, 
pneumonia  comes  on  insidiously,  sudden  prostration  and 
a  comatose  state  being  the  first  symptoms  observed. 

Following  the  chill,  usually  there  is  pain  underneath  the 
nipple  of  the  affected  side ;  this  pain,  however,  is  not  con- 
stant, neither  is  it  characteristic,  for  it  does  not  depend 
upon  the  pneumonic  process,  but  upon  the  accompanying 
pleurisy,  and  if  the  pneumonia  is  central,  and  does  not  in- 
volve the  surface  of  the  lung,  it  will  not  be  present.  This 
pain,  when  present,  is  increased  by  coughing  and  by  a  full 
inspiration ;  it  usually  subsides  within  three  or  four  days, 
and  is  almost  certain  not  to  continue  beyond  the  eighth 
day ;  if  pain  in  the  affected  side  continues  beyond  the 
sighth  day,  it  may  be  regarded  as  an  evidence  of  pleuro- 
pneumonia. 

In  no  other  acute  disease  is  the  respiration  so  constantly 
increased  in  frequency  as  in  this ;  it  is  rarely  less  than 
thirty  per  minute,  and  it  often  reaches  eighty.  The  in- 
creased frequency  of  the  pulse  does  not  correspond  to  the 


PNEUMONIA.  129 

increased  frequency  in  respiration  ;  it  is  not  uncommon  for 
the  latter  to  be  eighty  per  minute,  while  the  pulse  does  not 
rise  above  one  hundred. 

Dyspnoea  is  by  no  means  a  constant  attendant,  and,  when 
urgent,  does  not  seem  to  be  in  proportion  to  the  amount  of 
lung  involved,  for  often  there  is  less  frequency  in  respira- 
tion, and  less  dyspnoea  when  an  entire  lung  is  involved, 
than  when  only  a  small  portion  is  implicated. 

As  a  rule,  those  cases  which  are  accompanied  by  great 
nervous  prostration  suffer  most  from  dyspnoea.  Extreme 
dyspnoea  may  always  be  regarded  as  a  symptom  of  grave 
import.  The  dyspnoea  of  pneumonia  differs  very  markedly 
from  that  of  bronchitis ;  in  pneumonia  it  is  of  a  panting 
character,  while  in  bronchitis  it  is  labored,  and  there  is  a 
constant  muscular  effort  on  the  part  of  the  patient  to  force 
air  into  the  lungs. 

To  one  familiar  with  the  dyspnoea  of  the  two  diseases,  the 
difference  in  their  character  is  often  sufficient  for  a  differen- 
tial diagnosis. 

Cough  is  almost  a  constant  symptom  ;  it  usually  comes  on 
a  few  hours  after  the  accession  of  the  disease.  For  the  first 
twenty-four  hours,  if  there  is  any  expectoration,  it  is  simply 
bronchial  mucus  ;  after  this  time,  the  cough  will  be  accom- 
panied by  an  expectoration  which  is  peculiar ;  it  is  spoken 
of  as  the  ' '  characteristic  expectoration  of  pneumonia  ;  "  it 
is  gelatinous,  viscid,  tenacious,  and  semi-transparent,  never 
opaque.  Its  color  varies,. but  its  microscopical  appearances 
are  always  the  same  ;  it  is  composed  of  the  same  anatomical 
elements  already  described  as  filling  the  air-cells.  It  ad- 
heres so  closely  to  the  walls  of  the  vessel  which  contains  it, 
that  the  vessel  may  be  everted  without  displacing  it.  Its 
color  is  sometimes  of  a  cream-yellow,  at  other  times  of  a 
brick-dust  or  prune-juice  hue ;  this  latter  color  indicates 
extensive  blood  changes,  and  is  always  of  grave  import.  If 
a  case  is  tending  to  a  fatal  termination,  the  expectoration 
becomes  scanty,  less  tenacious,  and  of  a  greenish  color.  If, 
on  the  other  hand,  resolution  is  about  to  take  place,  it 
assumes  a  creamy  appearance,  and  is  profuse.  In  some 
cases,  when  the  other  rational  and  physical  signs  are  well 


130  SYMPTOMS. 

marked,  no  expectoration  occurs  throughout  the  whole 
course  of  the  disease.  Such  cases  are  most  frequently  met 
in  connection  with  acute  articular  rheumatism.  Expectora- 
tion may  also  be  wanting  in  the  pneumonia  of  the  aged. 

Countenance. — In  the  majority  of  cases,  the  aspect  of  the 
countenance  is  characteristic  of  the  disease ;  it  is  more  or 
less  flushed  and  anxious,  and  assumes  a  dusky  tint  tending 
in  some  cases  to  lividity,  which  is  usually  circumscribed  on 
the  cheeks,  and  may  be  compared  to  a  color  approaching 
mahogany.  It  more  closely  resembles  the  appearance  of 
the  countenance  in  typhus  fever  than  in  any  other  disease  ; 
with  this  exception,  that  in  typhus  fever  the  eye  is  dull, 
and  there  is  an  expression  of  stupidity  rather  than  anxiety. 

On  the  second  and  third  days  of  the  disease,  herpes  fre- 
quently make  their  appearance  on  the  face  and  about  the 
mouth.  In  severe  cases  the  lips  become  blue. 

Rise  in  temperature,  as  determined  by  the  thermometer 
in  the  axillae,  is  one  of  the  most  important  and  constant 
attendants  of  this  disease.  The  sudden  and  considerable 
rise  which  marks  its  invasion  reaches  102°  F.,  103°  F.,  105°  F., 
or  even  higher  by  the  second  or  third  day, — the  maximum  is 
generally  reached  by  the  evening  of  the  third  day.  Usually, 
there  are  slight  fluctuations  within  the  first  twenty-four 
hours,  but  they  have  no  regular  period  of  rise  and  fall. 
Generally,  the  temperature  is  lowest  early  in  the  morning, 
begins  to  rise  in  the  forenoon,  and  attains  its  maximum 
early  in  the  evening ;  these  morning  and  evening  fluctua- 
tions rarely  exceed  more  than  a  degree. 

In  some  cases,  where  the  patient  has  recovered,  but  more 
frequently  in  fatal  cases,  the  temperature  has  been  known  to 
rise  as  high  as  107°  F.  In  uncomplicated  cases,  during  the 
first  week  the  temperature  usually  ranges  from  102°  F.  to 
103°  F.  ;  it  is  seldom  higher  than  104°  F.,  and  in  a  large 
number  of  cases  it  does  not  reach  103°  F. 

The  first  indication  of  convalescence  is  a  fall  of  two  or 
three  degrees  in  temperature.  The  critical  day  of  this  dis- 
ease, as  regards  temperature,  is  the  fifth.  In  uncom- 
plicated cases,  the  temperature  falls  a  degree  or  two  on  the 
fifth  day  ;  if  the  decline  is  gradual  it  reaches  its  minimum 


PNEUMONIA.  131 

by  the  ninth  ;  for  a  number  of  days  after  the  decline  has 
commenced  there  is  a  tendency  to  temporary  exacerbations 
from  slight  causes.  If  resolution  takes  places  by  crisis,  the 
temperature  sometimes  falls  five  or  six  degrees  in  twenty- 
four  hours.  If  relapses  occur,  they  occur  within  three  or 
four  days  succeeding  the  crisis,  and  they  are  marked  by 
another  sudden  rise  in  temperature. 

A  high  temperature  after  the  tenth  day  indicates  that  the 
pneumonic  inflammation  is  extending,  or  that  purulent 
infiltration  is  taking  place.  The  days  of  crisis  in  uncom- 
plicated cases  are  the  fifth,  sixth,  and  seventh  /  neither  the 
height  of  the  temperature  nor  the  amount  of  lung  involved 
delays  the  period  of  crisis.  Pneumonia  at  the  apex  of 
the  lung  reaches  a  higher  temperature  and  is  maintained 
for  a  longer  period  than  when  it  has  its  seat  at  the  base  of 
the  lung.  With  the  decline  in  temperature,  the  whole 
aspect  of  the  patient  is  markedly  changed, — the  flush  dis- 
appears from  the  face,  and  the  patient  breaks  out  in  a  pro- 
fuse perspiration  ;  now  he  is  fully  convalescent. 


LECTURE    XI. 


PNEUMONIA. 

Croupous  or  Lobar  Pneumonia  (continued.) 

I  WILL  continue  the  history  of  the  symptoms  of  croupous 
pneumonia  by  inviting  your  attention  to  the  variations  in 
the  pulse.  The  pulse  of  pneumonia  varies  with  the  severity 
and  extent  of  the  pneumonic  inflammation,  and  with  the 
stage  of  the  disease.  In  cases  of  moderate  severity  it 
ranges  from  90  to  120  beats  per  minute,  but  it  may  reach 
140  or  even  160  in  severe  cases  ;  it  reaches  its  maximum  fre 
quency  by  the  fifth  day  of  the  disease,  and  its  rapidity  is 
in  direct  ratio  with  the  extent  and  severity  of  the  pneumo- 
nia. In  those  cases  which  are  not  severe,  the  pulse  at  the 
onset  is  strong,  full,  and  incompressible ;  afterward  it 
becomes  feeble  in  character.  Whenever  the  respirations 
are  very  frequent  and  the  pulmonary  circulation  much 
oppressed,  the  pulse  is  small,  frequent,  and  feeble.  A  pulse 
over  120  per  minute  for  three  consecutive  days  indicates 
danger.  By  carefully  comparing  the  hourly  variations  of 
pulse  and  temperature  in  a  typical  case  of  pneumonia,  it  is 
evident  that  there  is  a  close  connection  between  them,  for  a 
fall  or  rise  in  one  will  be  followed  by  a  corresponding  fall  or 
rise  in  the  other.  A  high  temperature  is  accompanied  by  a 
rapid,  feeble  pulse,  and  a  low  temperature  by  a  moderately 
frequent,  full  pulse.  As  a  rule,  when  the  temperature  falls, 
the  pulse  also  falls  ;  this  holds  true  in  mild  as  well  as  in 
severe  cases.  An  intermittent  pulse  is  rarely  met  with  ex- 
cept in  old  age,  or  in  those  who  are  prematurely  old, — in 


PNEUMONIA.  133 

the  young  and  in  children  the  pulse  may  be  frequent  and 
irregular,  but  it  is  never  intermittent.  An  intermitting 
pulse  therefore  indicates  great  feebleness  of  vital  power. 
The  sphygmograph  is  often  very  useful  in  determining  the 
exact  characteristics  and  variations  of  the  pulse  in  pneu- 
monia, and  is  regarded  by  some  as  of  special  service  as  an 
element  of  prognosis,  and  in  the  record  of  cases. 

The  cerebral  symptoms  are  not  very  significant  in  the 
early  stage.  Headache  may  be  present  early  and  continue 
throughout  the  active  progress  of  the  disease.  Delirium 
and  convulsions  rarely  occur  except  in  debilitated  sub- 
jects, and  in  persons  of  dissipated  habits.  Delirium  is 
most  frequently  met  with  in  connection  with  alcoholismus, 
and  then  it  assumes  very  much  the  character  of  delirium 
tremens :  it  is  an  active,  busy,  restless  delirium  ;  occasion- 
ally it  becomes  so  violent  as  to  render  resort  to  phys- 
ical restraint  necessary.  Under  these  circumstances  it  is 
associated  with  muscular  tremors  or  subsultus, — it  indi- 
cates extensive  blood  changes.  Whenever  you  meet  with 
this  form  of  delirium  in  pneumonia,  it  behooves  you  to 
make  careful  and  diligent  search  into  the  former  habits  of 
your  patient,  without  regard  to  his  present  associations. 

In  children  the  cerebral  disturbance  may  resemble  that 
attending  meningitis, — marked  by  headache,  great  prostra- 
tion, delirium,  and  sometimes  by  rigidity  of  the  muscles  of 
the  back  of  the  neck.  Under  these  circumstances  the  pneu- 
monia is  liable  to  be  overlooked  and  mistaken  for  cerebro- 
spinal  meningitis.  These  symptoms  are  most  likely  to 
occur  in  connection  with  the  development  of  pneumonia  in 
children  from  five  to  seven  years  of  age. 

Symptoms  referable  to  the  digestive  organs  are  not  very 
important,  neither  are  they  of  service  in  the  diagnosis  ;  there 
is  always  loss  of  appetite,  and  not  unfrequently  nausea  and 
vomiting  are  present  from  the  very  onset  of  the  disease. 

The  tongue  varies  in  appearance  ;  sometimes  it  shows  but 
little  alteration,  but  usually  it  is  covered  with  a  thick  creamy 
coating.  In  severe  cases  it  becomes  brown  and  dry,  sordes 
collect  on  the  teeth,  and  the  lips  are  brown  and  cracked.  A 
brown,  dry  tongue  ordinarily  accompanies  a  frequent  feeble 


134  SYMPTOMS. 

pulse.  When  convalescence  commences,  generally  the 
tongue  becomes  clean,  and  the  appetite  returns. 

Loss  of  strength  occurs  earlier,  and  is  more  marked  in 
pneumonia  than  in  any  other  acute  disease,  except  typhus 
fever  ;  usually  the  patient  becomes  very  weak  within  four 
or  five  days,  but  generally  during  convalescence  the  recovery 
of  strength,  as  well  as  of  flesh,  is  very  rapid. 

In  the  majority  of  cases,  the  urine  is  scanty,  high-colored, 
and  of  high  specific  gravity.  The  changes  in  its  constituents 
do  not  differ  materially  from  those  in  other  acute  inflamma- 
tory diseases.  The  diminution  of  the  chlorides,  concerning 
which  much  has  been  written,  is  by  no  means  peculiar  to 
this  disease. 

During  any  stage,  albumen,  in  small  quantity,  may  ap- 
pear temporarily  in  the  urine,  although  it  is  most  frequently 
met  with  during  the  second  stage  of  the  disease.  A  small 
quantity  of  albumen  in  the  urine  may  be  regarded  as  one  of 
the  ordinary  phenomena  of  pneumonia,  probably  produced 
by  the  same  cause  as  the  pneumonia.  To  a  certain  extent, 
its  presence  is  indicative  of  some  blood  poison.  Usually, 
cases  in  which  there  is  a  considerable  amount  of  albumen 
are  more  severe  and  more  liable  to  be  fatal. 

The  symptoms  which  I  have  already  detailed  are  present 
in  nearly  all  cases,  but  they  may  not  all  be  prominent. 

Usually,  this  disease  runs  a  regular  course  :  it  is  ushered 
in  by  a  distinct  chill,  which  is  followed  by  a  rapid  rise  in 
temperature,  and  an  acceleration  of  pulse  ;  the  characteris- 
tic symptoms  of  the  disease  already  referred  to  go  on  devel- 
oping and  increasing  in  severity  until  the  critical  day,  the 
fifth  or  sixth  after  the  chill,  when  a  striking  change  takes 
place  in  the  whole  phenomena  of  the  disease  ;  the  tempera- 
ture and  pulse  fall  gradually  or  rapidly,  the  dyspnoea  abates, 
the  blood  disappears  from  the  sputa  (sometimes  suddenly), 
it  becomes  more  copious,  loses  its  tenacity  and  transparency, 
and  is  muco-purulent,  or  of  a  creamy  consistency.  Often 
in  twenty -four  hours  convalescence  is  fully  established,  the 
patient  not  unfrequently  passes  into  a  quiet,  natural  sleep, 
and  wakes  with  a  desire  for  food,  complaining  only  of  ex- 
treme exhaustion.  Tf,  however,  the  crisis  does  not  occur  on 


PNEUMONIA.  135 

the  days  mentioned,  but  the  temperature  remains  as  high,  or 
even  higher  than  at  any  previous  period,  perhaps  reaching 
and  continuing  for  a  few  days  at  106°  F.  or  107°  F.,  accom- 
panied by  great  prostration,  a  small,  rapid,  and  feeble  pulse, 
more  or  less  cerebral  disturbance,  with  a  tendency  to  stupor 
or  to  delirium,  the  tongue  becoming  dry  and  brown  ;  then 
we  have  the  disease  assuming  a  typhoid  character,  termed 
"typhoid  pneumonia,"  and  under  these  circumstances  the 
inflammatory  processes  do  not  run  their  regular  course. 
These  symptoms  indicate  the  occurrence  of  purulent  infiltra- 
tion of  the  consolidated  lung-tissue,  or  a  rapid  extension  of 
the  pneumonic  process,  or  very  extensive  blood  changes. 
Pneumonia  secondary  to  or  complicated  by  other  diseases 
is  very  liable  to  assume  this  type. 

In  the  pneumonia  of  old  people,  and  persons  of  depraved 
constitution,  typhoid  symptoms  may  develop  early  in  the 
disease,  indeed  they  may  be  present  at  the  very  onset  of  the 
pneumonia.  This  variety  is  often  unattended  by  cough, 
expectoration,  or  any  of  the  other  rational  symptoms. 
The  majority  of  the  cases  of  this  form  of  asthenic  pneumo- 
nia terminate  fatally,  but  recovery  is  always  possible  ;  occa- 
sionally on  the  fourteenth  or  fifteenth  day  convalescence 
commences,  and  after  a  slow  and  extremely  tedious  conva- 
lescence, complete  recovery  may  be  reached. 

The  pneumonia  which  complicates  acute  alcholismus  is 
very  apt  to  pass  unrecognized  unless  frequent  physical 
examinations  of  the  chest  are  made. 

The  importance  of  frequent  thermometrical  observations 
in  all  cases  of  delirium  tremens,  as  well  as  in  all  other 
diseases  in  which  pneumonia  is  liable  to  occur  as  a  compli 
cation,  cannot  be  over-estimated,  for,  as  I  have  already 
stated,  there  is  no  other  disease  which  is  so  uniformly 
marked  by  a  sudden  rise  of  temperature. 

I  will  now  pass  to  the  examination  of  the  physical  signs. 

PHYSICAL  SIGNS. — The  physical  signs  indicative  of  pneu- 
monia usually  make  their  appearance  within  twenty-four 
hours  after  its  invasion  ;  although,  if  it  is  central,  they  may 
not  be  present  during  the  first  two  or  three  days.  By  con- 
sidering these  signs  in  connection  with  the  anatomical  stages 


136  PHYSICAL   SIG]STS. 

of  the  disease,  their  importance  in  a  diagnostic  and  prog- 
nostic point  of  view  can  be  better  appreciated. 

In  the  first  stage,  or  stage  of  engorgement,  on  inspection 
the  movements  of  the  affected  side  are  noticed  to  be  some- 
what restrained, — on  palpation  there  may  be  a  slight  in- 
crease of  the  vocal  fremitus  on  the  affected  side  ;  as  a  rule, 
however,  in  this  stage,  inspection  and  palpation  are  nega- 
tive in  their  results. 

On  percussion,  slight  dulness  is  present  over  so  much  of 
the  lung-tissue  as  is  involved  in  the  pneumonic  inflamma- 
tion ;  the  degree  and  extent  of  the  dulness  correspond  to 
the  amount  of  exudation  into  the  lung  substance. 

On  auscultation,  if  practised  early,  the  respiratory  mur- 
mur will  be  found  feeble  over  the  affected  portion  of  lung, 
and  it  will  have  an  unnatural  dry  ness :  this  is  the  dry 
stage  referred  to  by  Dr.  Stokes  ;  it  is  the  stage  of  congestion 
before  there  is  any  exudation  into  the  air-cells.  This  con- 
dition only  exists  very  early  and  is  not  often  recognized. 

As  soon  as  there  is  any  exudation  into  the  air-cells,  fine 
crackling  sounds  are  heard  at  the  end  of  inspiration  ;  these 
sounds  are  termed  crepitant  rales,  and  are  regarded  as  the 
characteristic  sign  of  the  first  stage  of  pneumonia, — they 
are  not  changed  by  coughing,  but  remain  audible  over  a 
circumscribed  space  from  twelve  to  twenty -four  hours. 

In  some  cases,  especially  when  pneumonia  is  developed 
in  connection  with  acute  articular  rheumatism,  crepitation 
never  occurs. 

The  vocal  sounds  are  usually  slightly  increased  in  in- 
tensity. 

In  the  second  stage,  or  stage  of  red  Tiepatization,  the 
physical  evidences  furnished  by  inspection  and  palpation 
are  more  important. 

By  inspection  it  will  be  seen  that  the  expansive  move- 
ments of  the  affected  side  are  more  markedly  diminished 
than  in  the  first  stage,  while  those  of  the  healthy  side  are 
increased. 

By  palpation,  it  will  be  found  that  there  is  a  marked 
increase  in  the  vocal  fremitus  on  the  affected  side  over  the 
consolidated  lung-tissue. 


PNEUMONIA.  131 

On  percussion,  there  will  be  marked  dulness  over  so 
much  of  the  lung  as  is  the  seat  of  the  pneumonia,  while 
over  the  healthy  portion  of  the  affected  lung,  as  well  as 
over  the  opposite  lung,  there  will  be  exaggerated  pul- 
monary resonance.  The  line  of  dulness  is  not  affected  by 
a  change  in  the  position  of  the  patient ;  absolute  dulness  or 
flatness  on  forcible  percussion  very  rarely  exists. 

On  auscultation,  bronchial  respiration  will  be  heard  over 
the  affected  portion  of  lung ;  the  crepitant  rale  of  the  first 
stage  gives  place  to  the  tubular  breathing,  for  the  reason 
that  when  the  crepitant  rales  were  heard,  the  air-cells  were 
only  partially  filled ;  but  now  the  air-cells  are  filled  with 
solid  material,  which  excludes  the  vesicular  element  of  res- 
piration, and  the  consolidated  lung  being  a  good  conduct- 
ing medium,  the  bronchial  element  of  respiration  is  conveyed 
to  the  surface.  The  more  complete  the  consolidation,  the 
more  intense  and  tubular  is  the  bronchial  respiration.  The 
heart-sounds  over  the  consolidated  portion  of  lung  are 
transmitted  to  the  surface  with  unnatural  intensity. 

The  voice- sounds  are  increased  in  intensity,  and  are  bron- 
chophonic  in  character  over  all  that  portion  of  lung  which  is 
the  seat  of  the  consolidation. 

There  are,  therefore,  three  characteristic  physical  signs  of 
the  second  stage  of  pneumonia,  viz.,  dulness  on  percus- 
sion, broncliial  respiration,  and  increased  vocal  fremitus, 
and  resonance. 

In  the  third  stage,  or  stage  of  gray  Tiepatization,  the 
physical  signs  at  first  are  unchanged  ;  during  the  early  part 
of  this  stage  they  are  the  same  as  those  of  the  second  stage  ; 
when  resolution  commences,  expansive  motion  on  the 
affected  side  becomes  more  and  more  apparent  as  the  resolu- 
tion goes  on,  vocal  fremitus  as  well  as  vocal  resonance  be- 
comes less  and  less  marked. 

Percussion  shows  progressive  diminution  in  dulness, — it 
is,  however,  a  long  time  before  normal  pulmonary  resonance 
is  completely  restored. 

On  auscultation,  the  bronchial  respiration  of  the  second 
stage  gradually  gives  place  to  rude  or  broncho-vesicular  res- 
piration, and  this  in  turn  approximates  to,  and  at  length 


138  PHYSICAL   SIGNS. 

ends  in  normal  vesicular  breathing.  As  the  bronchial  res- 
piration diminishes,  the  crepitant  and  subcrepitant  rales,  or 
"rales  redux,"  are  developed,  accompanied  by  mucous 
rales  of  large  and  small  size  ;  these  remain  audible  until 
resolution  is  complete. 

BronchopTiony  gives  place  to  exaggerated  vocal  resonance, 
and  this  in  turn  to  normal  vocal  resonance. 

No  one  of  the  physical  signs  which  I  have  detailed  to  you 
as  occurring  in  the  different  stages  of  pneumonia,  is  suffi- 
cient to  enable  you  to  make  a  positive  diagnosis  of  its  exist- 
ence ;  a  concurrence  of  all  these  different  physical  signs  is 
alone  sufficient  for  the  physical  diagnosis  of  pneumonia. 

When  the  temperature  falls,  and  there  is  a  corresponding 
diminution  in  the  frequency  of  the  pulse  and  respiration, 
bronchial  breathing  is  heard  over  the  inflamed  lung-tissue, 
and  you  may  then  accurately  note  the  progress  of  the  reso- 
lution by  the  development  of  the  physical  signs  of  the  reso- 
lution. If,  however,  the  softening  and  resolution  do  not 
take  place  at  the  regular  period  for  their  occurrence,  the 
temperature  remains  high,  and  symptoms  of  prostration  are 
developed,  indicating  purulent  infiltration.  Under  such 
circumstances,  bronchial  respiration  will  continue  and  be- 
come more  intense,  the  air-cells  becoming  more  distended  by 
the  rapid  cell-formation, — dulness  on  purcnssion  becomes 
more  and  more  marked,  until  finally,  when  rales  occur,  they 
are  high-pitched,  and  very  closely  resemble  fine  gurgles  ;  if 
softening  takes  place,  and  abscesses  form,  similar  high- 
pitched  metallic  rales  will  be  heard  over  circumscribed 
places  ;  these  resemble  in  character  subcrepitant  rales. 

The  process  of  resolution  may  be  developed  in  other  ways 
— the  temperature  may  fall  on  the  seventh  or  eighth  day  of 
the  disease,  but  the  dulness  on  percussion,  and  the  bron- 
chial respiration  continue,  the  "rales  redux"  do  not  ap- 
pear,— the  patient  feels  better,  but  the  physical  signs  of 
resolution  do  not  develop.  This  condition  of  things  is  very 
likely  to  occur  in  cases  of  pleuro-pneumonia,  also  in  that 
class  of  patients  whose  vitality  is  low. 

The  physical  signs  of  the  third  stage  may  sometimes  con- 
tinue two  or  three  weeks  after  all  the  rational  symptoms  of 


PNEUMONIA.  139 

the  disease  have  disappeared  ;  in  these  cases  of  slow  reso- 
lution, the  lung  will  always  be  more  or  less  permanently 
crippled,  or,  at  least,  a  long  time  will  elapse  before  it  will 
perform  its  natural  function. 

DIFFERENTIAL  DIAGNOSIS. — In  most  cases,  the  diagnosis 
of  acute  lobar  pneumonia  is  not  difficult,  if  the  physical 
signs  and  rational  symptoms  are  properly  appreciated.  If, 
however,  it  occurs  in  a  child,  or  in  an  aged  person,  or  in  a 
debilitated,  broken-down  constitution,  it  may  pass  unrecog- 
nized. In  children,  the  convulsions  which  usher  it  in,  the 
absence  of  cough  and  expectoration,  and  the  high  fever,  lead 
to  the  diagnosis  of  cerebral  disease.  In  the  aged  and  de- 
bilitated, the  typhoid  symptoms,  and  the  absence  of  tho- 
racic symptoms,  lead  to  the  diagnosis  of  fever.  In  both 
instances,  a  careful  physical  examination  of  the  chest  will 
lead  to  a  correct  diagnosis.  The  differential  diagnosis 
between  pneumonia  and  pleurisy  rests  mainly  upon  the 
following  points.  Generally,  pneumonia  is  ushered  in  by  a 
distinct  chill,  while  pleurisy  rarely  commences  with  a  dis- 
tinct chill ;  in  pleurisy  there  are  no  critical  days,  which  are 
observed  in  almost  every  case  of  pneumonia.  Usually, 
there  is  but  little  cough  or  expectoration  in  pleurisy,  while 
pneumonia  is  almost  always  accompanied  by  a  cough  with 
a  characteristic  expectoration.  In  pleurisy  the  tempera- 
ture ranges  much  lower  than  in  pneumonia.  The  counte- 
nance of  pleurisy  is  pale  and  anxious,  while  in  pneumonia 
it  is  flushed  and  perhaps  turgid.  In  pleurisy  the  breathing 
is  catching  in  character,  while  in  pneumonia  the  respirations 
are  increased  in  frequency,  but  not  necessarily  catching  in 
character.  In  pneumonia  the  presence  of  crackling  rales, 
bronchial  respiration,  dulness  on  percussion,  and  in- 
creased vocal  fremitus  and  resonance,  are  usually  sufficient 
for  a  diagnosis,  although  in  some  cases  of  extreme  pleuritic 
effusion  the  presence  of  bronchial  breathing  may  lead  to  the 
diagnosis  of  the  second  stage  of  pneumonia.  It  is  for  this 
reason  that  mistakes  are  sometimes  made  in  the  differential 
diagnosis  between  these  diseases.  Pleurisy  with  bronchial 
breathing  is  much  more  likely  to  be  mistaken  for  pneumo- 
nia, than  the  second  stage  of  pneumonia  is  to  be  mistaken  for 


140  PKOGHSTOSig. 

pleurisy.  In  some  cases,  the  distinction  is  not  easily 
and  the  greatest  care  will  be  required  in  making  the  examina- 
tion. It  will  be  remembered,  that  in  pleurisy  the  percussion 
sound  assumes  a  flatness  which  is  not  present  in  the  second 
stage  of  pneumonia.  In  pleurisy  there  is  an  entire  absence 
of  vocal  fremitus  and  vocal  resonance  upon  the  affected  side, 
while  in  pneumonia  the  vocal  fremitus  is  increased,  and  the 
vocal  sounds  are  intensified.  It  is  by  the  presence  of  vocal 
fremitus,  absence  of  flatness  upon  percussion,  and  the 
rational  symptoms  developed  in  the  history  of  the  case, 
that  the  pneumonia  will  be  recognized,  when  the  question 
of  differential  diagnosis  arises  between  it  and  pleurisy  with 
effusion. 

The  third  state  of  pneumonia  may  be  confounded  with 
capillary  bronchitis,  for  subcrepitant  rales  are  present  in 
both  ;  but  capillary  bronchitis  is  not  necessarily  ushered  in 
with  a  chill,  and  the  temperature  never  ranges  so  high  as  in 
pneumonia ;  besides,  the  dulness  on  percussion  and  the 
bronchial  character  of  the  respiration  which  is  present  over 
consolidated  lung-tissue  is  absent  in  capillary  bronchitis. 
The  subcrepitant  rales  of  bronchitis  are  heard  over  the 
entire  chest,  while  in  pneumonia  they  are  confined  to  a 
circumscribed  space.  When  the  characteristic  rusty  expec- 
toration of  pneumonia  is  present,  the  question  of  diagnosis 
is  readily  settled. 

In  most  instances,  pneumonia  can  be  distinguished  very 
readily  from  pulmonary  O3dema  by  the  rational  symptoms, 
for,  although  the  physical  signs  of  the  first  stage  of  pneu- 
monia very  closely  resemble  those  present  in  pulmonary 
oedema,  the  presence  of  the  chill,  fever,  pain  in  the  side, 
and  the  characteristic  expectoration  which  attends  the  de- 
velopment of  the  pneumonia,  are  sufficient  to  distinguish  it 
from  pulmonary  oedema.  There  are  other  diseases  with 
which  acute  pneumonia  is  occasionally  confounded,  to 
which  reference  has  already  been  made,  so  that  they  hardly 
require  separate  consideration. 

PROGNOSIS. — The  prognosis  in  pneumonia  depends  more 
upon  the  age  of  the  patient  than  upon  any  other  single 
element :  occurring  in  the  young  child,  or  in  a  very  old 


PNEUMONIA.  141 

person,  it  is  almost  certainly  fatal ;  between  the  ages  of 
40  and  70  the  death-rate  ranges  between  one  in  five  and  one 
in  seven  ;  its  lowest  rate  of  mortality  is  between  the  ages  of 
10  and  30 ;  the  majority  of  uncomplicated  cases  occurring 
between  these  ages  will  recover.  The  prognosis  is  also  in- 
fluenced greatly  by  the  extent  of  the  disease  ;  double  pneu- 
monia is  very  generally  fatal  ;  when  an  entire  lung  is  involv- 
ed, it  is  more  dangerous  than  when  it  is  confined  to  one  lobe. 

Chronic  alcoholismus,  and  feebleness  of  constitution,  either 
from  excesses  or  from  anti-hygienic  influences,  tend  to  ren- 
der the  prognosis  unfavorable  ;  habitual  drunkenness  must 
always  be  regarded  as  imparting  special  danger  to  pneu- 
monia. Certain  epidemic  influences  are  of  the  utmost  im- 
portance in  estimating  the  prognosis  in  pneumonia :  during 
some  seasons,  the  rate  of  mortality  is  small,  while,  during 
other  seasons,  the  disease  is  exceedingly  fatal. 

When  pneumonia  is  complicated  by  cardiac  disease, 
Bright' s  disease,  or,  in  fact,  by  any  serious  organic  disease, 
the  prognosis  is  unfavorable. 

The  condition  of  pregnancy  renders  pneumonia  partic- 
ularly dangerous;  although  it  may  involve  only  a  single 
lobe,  it  is  attended  with  very  great  danger. 

The  individual  symptoms  which  are  of  special  importance 
in  deciding  the  question  of  prognosis,  are  the  following : 
a  temperature  of  104°  F.  must  be  regarded  as  the  limit  in  a 
mild  case  of  pneumonia  ;  an  elevation  of  temperature  above 
106°  F.,  for  two  consecutive  days,  accompanied  by  a  pulse 
of  120  per  minute,  renders  the  prognosis  unfavorable.  A 
gradual  rise  in  temperature  after  the  fourth  day  is  always 
an  unfavorable  symptom ;  if  the  pulse  reaches  150  beats  per 
minute,  the  case  is  almost  certain  to  be  fatal.  Copious, 
liquid,  prune-juice  expectoration,  indicates  danger,  but  is 
not  necessarily  of  fatal  significance ;  but  absence  of  expec- 
toration in  the  second  and  third  stage  of  the  disease,  with 
loud  trachea!  rales,  indicates  rapidly  approaching  dissolu- 
tion. Marked  disturbances  of  the  nervous  system  always 
indicate  a  serious  form  of  pneumonia.  Delirium,  coming 
on  at  the  end  of  the  first  week,  especially  when  habits  of 
drinking  have  preceded  the  attack,  is  always  indicative  of 


142  PEOGN^OSIS. 

danger ;  mild  delirium  in  the  earlier  stages  of  the  disease  is 
not  uncommon,  and  has  no  serious  import.  In  old  people 
the  development  of  subsultus  tendinum,  and  a  tendency  to 
coma,  at  any  stage  of  the  disease  is  dangerous.  Extreme 
prostration,  accompanied  by  sunken,  pallid  countenance, 
followed  by  perspiration  which  is  cold  and  clammy  in  char- 
acter, in  whatever  stage  it  may  occur,  is  usually  attended 
with  great  danger. 

The  occurrence  of  pulmonary  congestion  and  oedema  in 
the  unaffected  portions  of  lung,  is  not  unfrequently  the 
direct  cause  of  death  ;  consequently,  it  becomes  an  element 
of  unfavorable  prognosis. 


LECTURE    XII. 


PNEUMONIA. 

Croupous  or  Lobar  Pneumonia  (continued.)  —  Catarrhal  or  Lobular  Pneu- 
monia. 

TKEATMENT. — At  the  close  of  my  last  lecture  I  completed 
the  history  of  croupous  pneumonia,  with  the  exception  of 
its  treatment.  Perhaps  there  is  no  disease,  the  treatment 
of  which  has  been  so  bitterly  and  earnestly  discussed,  as  the 
one  now  under  consideration.  It  has  been  "the  battle-field 
of  the  advocates  of  heroic  measures"  on  the  one  hand,  and 
of  the  advocates  of  "the  expectant  plan  of  treatment"  on 
the  other.  One  who  carefully  studies  the  natural  history 
of  the  disease  can  place  but  little  reliance  on,  or  attach  but 
little  value  to  any  plan  of  treatment,  as  regards  its  curative 
effects,  if  it  is  indiscriminately  employed.  The  natural  ten- 
dency of  pneumonia,  if  uncomplicated,  is  to  terminate 
spontaneously  in  a  crisis  between  the  fifth  and  sixth  day, 
and  when  we  take  into  consideration  the  effects  of  age,  sex, 
constitution,  and  certain  unknown  atmospheric  influences 
on  pneumonic  patients,  we  can  readily  understand  how 
difficult  it  is  to  estimate  the  relative  value  of  the  different 
methods  or  plans  of  treatment  which  have  been  resorted  to 
for  its  cure. 

There  are  periods  and  conditions  of  life  in  which  pneu- 
monia is  almost  certainly  fatal ;  and  on  the  other  hand, 
there  are  periods  of  life  and  conditions  in  which  a  patient 
with  pneumonia  is  almost  certain  to  recover. 

Although  there  can  be  but  little  doubt  that  a  large 


144  TREATMENT. 

number  of  cases  would  terminate  in  recovery  if  left  to 
themselves,  it  is  equally  certain  that  many  lives  may  be 
saved  by  the  judicious  use  of  therapeutic  measures  ;  and 
even  in  the  milder  cases,  the  duration  of  the  disease  may 
be  shortened  and  convalescence  hastened. 

Bear  in  mind  this  fact,  that  in  the  successful  manage- 
ment of  this  disease  your  duty  is  not  so  much  to  treat  the 
diseased  lung,  as  the  constitutional  condition  of  the  patient. 

The  plan  of  treatment  which  has  been  most  extensively 
employed  in  the  management  of  this  disease,  but  which  is 
now  almost  entirely  discarded,  is  general  blood-letting. 
Many  years  ago  no  one  would  have  ventured  to  treat  pneu- 
monia without  resorting  to  one  or  more  bleedings ;  but 
now  few,  if  any,  would  think  of  having  recourse  to  such  a 
practice. 

From  a  careful  review  of  the  written  history  of  venesec- 
tion in  pneumonia,  one  almost  necessarily  reaches  the 
following  conclusions  :  first,  that  indiscriminate  bleeding 
in  this  disease  increases  the  ratio  of  mortality,  as  it  is  now 
a  far  less  fatal  disease  than  when  blood-letting  was  em- 
ployed in  its  treatment ;  second,  that  there  is  no  evidence 
to  substantiate  the  opinion  that  blood-letting  has  the  power 
either  to  arrest  the  progress  or  diminish  the  severity  of  the 
pneumonia  ;  tliird,  that  blood-letting,  when  practised  upon 
the  old  or  young,  or  upon  debilitated  subjects,  greatly 
diminishes  the  chances  of  their  recovery.  These  are  con- 
clusions which  are  reached  simply  by  the  study  of  statis- 
tics. To  the  practical  observer  there  can  be  no  question 
but  that  free  blood-lettings  delay  the  period  of  convales- 
cence ;  the  critical  day  may  be  reached  as  early,  but  con- 
valescence is  prolonged,  as  recovery  is  more  rapid  when  it 
is  not  resorted  to.  In  the  strong  and  robust,  and  in  persons 
who  are  in  full  vigor  at  the  time  of  the  attack,  a  free  bleed- 
ing will  temporarily  relieve  the  urgent  symptoms ;  but  at 
the  same  time  it  will  diminish  the  chances  of  rapid  and 
complete  convalescence,  and  the  subsequent  dangers  of  the 
disease  are  greatly  increased  by  its  performance. 

There  is  one  condition  in  which  it  seems  to  me  that  a 
patient  with  pneumonia  may  be  bled  with  advantage,  and 


PNEUMONIA.  145 

that  is,  when  there  is  evidence  that  the  heart  is  engorged 
with  blood,  accompanied  by  the  evidences  of  sudden  pul- 
monary congestion  and  oadema.  Under  such  circumstances 
a  free  bleeding,  if  the  patient  is  vigorous,  will  unquestion- 
ably give  prompt  and  salutary  relief.  The  fact  that  an 
apparently  robust  person  has  pneumonia,  should  not  be 
taken  as  sufficient  evidence  that  blood-letting  is  to  enter 
into  the  treatment  of  the  case  ;  it  is  an  overcrowding  with 
blood  of  that  portion  of  the  lungs  which  is  not  the  seat  of 
the  pneumonia,  that  is  to  determine  the  question  of  blood- 
letting. 

Antimony  and  calomel  have  also  been  very  extensively 
employed  in  the  treatment  of  pneumonia,  but  these  reme- 
dies have  also  now  fallen  almost  entirely  into  disuse.  There 
is  no  evidence  that  they  possess  any  power  to  arrest  the 
progress  or  diminish  the  severity  of  the  disease  ;  calomel 
does  not  promote  the  absorption  of  the  material  which  fills 
the  air-cells,  as  was  once  claimed,  nor  does  antimony  in 
large  or  small  doses  have  the  power,  which  was  once  claimed 
for  it,  to  arrest  the  disease,  or  to  prevent  congestion  of  the 
unaffected  portion  of  lung. 

Veratrum  mride  and  aconite,  within  the  last  few  years, 
have  been  very  extensively  employed  in  the  treatment  of 
pneumonia.  Ifc  is  claimed  for  them  that  they  have  the 
power,  not  only  of  diminishing  the  frequency  of  the  pulse, 
but  of  lowering  the  temperature.  There  can  be  little  doubt 
but  that  both  of  these  drugs  temporarily  have  this  power, 
without  giving  rise  to  any  unpleasant  symptoms  ;  but,  if 
their  use  is  continued  for  a  day  or  two  in  sufficiently  large 
doses  to  accomplish  these  results,  they  seem  to  me  to  act 
unfavorably,  and  to  prejudice  the  chances  of  convalescence, 
as  they  are  apt  to  produce  vomiting  and  great  prostration, 
and  sometimes  collapse.  I  am  confident  that  they  decidedly 
interfere  with  the  nutrition  of  the  patient.  If  used  at  all, 
they  are  to  be  resorted  to  under  circumstances  similar  to 
those  in  which  perhaps  bleeding  might  be  practised  with 
benefit.  It  is  claimed  by  some  that  veratrum  viride  is  a 
cardiac  tonic,  and  for  that  reason  that  its  administration  is 
beneficial ;  but  digitalis  is  a  far  more  reliable  and  safe  heart- 

10 


146  TREATMENT. 

tonic  than  veratrum,  and  if  the  administration  of  any  drug 
is  desirable  on  that  account,  digitalis  should  have  the 
preference.  There  is  no  satisfactory  evidence  that  either  of 
these  agents  has  any  direct  influence  in  controlling  the 
inflammatory  processes. 

In  a  large  proportion  of  cases  of  pneumonia  occur- 
ring in  young  adults,  you  will  find  that  all  the  remedial 
agents  I  have  thus  far  mentioned  may  be  dispensed  with, 
the  disease  passing  rapidly  through  its  different  stages  to  a 
satisfactory  termination.  Rest  in  bed  in  a  large,  well-ven- 
tilated apartment,  the  temperature  of  which  ranges  between 
68°  F.  and  70°  F.,  with  the  free  administration  of  liquid  nutri- 
tious food,  such  as  milk,  eggs,  etc.,  is  all  that  is  required. 
If  the  patient  suffers  from  pain  in  the  affected  side,  a  hypo- 
dermic injection  of  morphine  will  give  the  most  speedy  and 
permanent  relief ;  if  the  cough  is  distressing,  opium  or 
chloral  in  small  doses  will  generally  allay  it.  If,  in  any 
case,  you  are  in  doubt  as  to  whether  any  remedial  agent 
should  be  employed,  give  the  patient  the  benefit  of  the 
doubt,  and  withhold  the  administration  of  drugs,  at  least 
until  the  time  when,  according  to  the  natural  history  of 
the  disease,  the  day  of  crisis  shall  be  reached. 

My  own  observation  has  led  me  to  the  conviction  that 
there  can  be  no  established  plan  of  treatment, — that  we  are 
not  to  treat  so  much  the  pneumonia  as  the  individual 
patient.  I  have  uniformly  adopted  the  principle  that 
nature  is  to  be  trusted  to  a  great  extent,  believing  that 
pneumonic  patients  are  more  likely  to  recover  under  no 
active  treatment,  than  under  a  routine  treatment  blindly 
followed. 

In  the  severer  types  of  pneumonia  occurring  in  enfeebled 
subjects,  it  has  appeared  to  me  that  there  are  two  sources 
of  danger,  viz.,  Tiigli  temperature,  and  feeble  Tieart-power ; 
the  latter  may  have  existed  prior  to  the  attack,  or  have 
been  developed  during  its  progress.  There  are,  conse- 
quently, two  prominent  indications  for  treatment, — the  re- 
duction of  temperature  and  the  sustaining  of  the  heart- 
power.  A  high  temperature  long  continued,  in  acute  disease 
destroys  life  by  the  changes  it  produces  in  the  constituents 


PNEUMONIA.  147 

of  the  blood,  while  feeble  heart-power  gives  rise  to  danger 
from  passive  pulmonary  congestion  and  the  commencing 
palsy  of  the  bronchial  muscles  which  impedes  the  evacua- 
tion of  the  bronchial  tubes.  I  have  already  referred  to 
those  means  which  have  usually  been  employed  for  the  re- 
duction of  temperature,  and  have  stated  my  objections  to 
their  use. 

The  Germans  believe  that  in  pneumonia  the  temperature 
can  be  reduced  by  the  application  to  the  chest  of  cold  com- 
presses,— a  cloth  of  some  thickness  is  to  be  wrung  from  cold 
water  and  applied  every  five  or  ten  minutes  to  the  affected 
side.  It  is  claimed  for  this  measure,  that  not  only  does  it 
relieve  the  local  symptoms,  but  it  lowers  the  body  temper- 
ature and  hastens  the  day  of  crisis.  There  can  be  no  doubt 
that  the  pain  in  the  side  and  the  dyspnoea  will  be  relieved 
in  this  way  ;  but  it  is  also  certain  that  the  reduction  of  tem- 
perature and  relief  of  local  symptoms  is  only  temporary. 
My  own  experience  would  lead  me  to  believe  that  pneu- 
monia treated  in  this  way  is  more  liable  to  extend  ;  besides, 
unless  great  care  is  exercised  in  the  application  of  the  com- 
press the  patient  is  quite  likely  to  be  chilled ;  therefore, 
on  account  of  the  slight  and  temporary  benefit  derived 
from,  and  the  dangers  that  may  attend  its  application,  it 
must  be  regarded  as  a  measure  not  adapted  to  general  use. 

Let  us  now  briefly  notice  the  cause  of  the  high  temper- 
ature which  is  present  in  pneumonia  as  well  as  in  other 
acute  inflammatory  diseases.  Unquestionably,  it  is  due  to 
the  rapid  molecular  metamorphosis  which  is  going  on  in 
the  body  ;  and  in  seeking  for  an  antipyretic,  if  possible, 
we  must  find  a  remedy  which  has  the  power  of  staying  this 
rapid  molecular  change.  The  pulse  may  be  made  slower 
by  the  use  of  veratrum  viride,  but  this  effect  is  only  tempo- 
rary ;  the  same  is  true  of  the  effect  produced  by  the  other 
means  which  have  been  mentioned,  which  have  been  ex- 
tensively employed  for  this  purpose.  In  the  sulphate  of 
quinine  I  believe  we  have  a  true  antipyretic ;  it  has  been 
claimed  that  this  remedy  is  an  arterial  sedative,  and  has  a 
peculiar  effect  upon  the  capillary  circulation ;  also  that  it 
has  the  power  of  arresting  cell-development  as  well  as  the 


148  TREATMENT. 

amoeboid  movement  of  the  white  globules.  Whether  its 
efficacy  is  due  to  one  or  all  of  these  actions  is  not  as  yet 
definitely  settled,  but  clinical  observation  has  established 
the  fact  that  it  has  the  power  of  permanently  reducing 
temperature  with  greater  certainty  than  any  other  remedial 
agent.  The  objection  to  all  the  other  measures  for  redu- ; 
cing  temperature  which  have  been  referred  to,  is  the  de- 
pression which  follows  their  use,  as  this  becomes  a  special 
element  of  danger  as  soon  as  the  critical  day  of  the  disease 
is  passed.  To  the  use  of  quinine  there  is  no  such  objection, 
for  by  its  action  on  the  nervous  system  it  increases  the 
power  of  the  heart' s  action,  and  so  avoids  the  second  danger 
of  the  disease. 

On  this  principle,  for  the  past  four  years  the  rule  of  prac- 
tice in  my  wards  in  Bellevue  Hospital  has  been  to  place  all 
patients  with  pneumonia  of  a  severe  type  on  the  sulphate 
of  quinine,  in  doses  varying  from  twenty  to  thirty  grains  per 
day,  and  it  is  the  exception  for  a  pneumonic  patient  not  to 
show  a  marked  reduction  of  temperature  within  thirty-six 
hours  after  the  commencement  of  its  use.  It  does  not 
seem  to  arrest  the  progress  of  the  pneumonia,  but  it  lowers 
temperature,  shortens  the  duration  of  the  febrile  stage,  and 
hastens  the  stage  of  resolution  to  complete  recovery. 

The  second  indication  of  treatment  is  feebleness  in  power 
of  the  heart's  action  ;  nearly  all  deaths  from  pneumonia 
result  directly  or  indirectly  from  a  failure  of  heart-power. 
It  is  not  the  heart-clot  that  kills,  but  the  antecedent  feeble- 
ness of  the  heart's  action,  which  permits  the  formation 
of  the  heart-clot.  The  pulmonary  osdema,  the  cyanosis, 
the  hurried  respiration,  which  are  often  present,  are  some 
of  the  results  of  deficient  heart-force,  and  constitute  a 
class  of  symptoms  which  demand  immediate  attention. 
The  most  serviceable  remedy  for  accomplishing  relief  is 
alcohol.  Alcoholic  stimulants,  judiciously  employed,  are 
among  the  most  efficient  means  which  we  possess  for  sus- 
taining the  heart-power  in  the  treatment  of  this  disease. 
There  are  cases  of  pneumonia  which  demand  the  use  of  stim- 
ulants, yet  the  indiscriminate  use  of  them  is  more  dan- 
gerous than  indiscriminate  blood-letting.  It  may  be  but  a 


PNEUMONIA.  149 

few  ounces  of  stimulants  which,  will  be  required  to  assist 
the  patient  through  an  emergency,  or  it  may  be  the  regular 
and  free  administration  of  the  agent  which  is  to  save  life. 
In  the  old  and  feeble,  and  in  persons  who  have  been  accus- 
tomed to  the  use  of  alcohol,  stimulants  may  be  indicated 
from  the  very  commencement  of  the  attack,  and  their  use 
required  throughout  the  course  of  the  disease. 

In  a  large  number  of  cases,  one  of  the  chief  duties  of  the 
physician  is  to  watch  carefully  for  the  symptoms  indicating 
the  employment  of  stimulants.  The  state  of  the  pulse,  which 
very  accurately  determines  the  amount  of  heart-power,  is 
the  safest  guide  ;  as  a  rule,  an  extremely  rapid,  feeble  pulse, 
beating  120  or  130  times  per  minute,  calls  for  stimulants. 
It  is  advisable  to  commence  their  use  in  small  doses,  and 
carefully  watch  the  effect ;  if  it  is  to  be  beneficial,  a  favor- 
able result  will  follow,  generally  within  a  few  hours  ;  after 
this,  the  quantity  to  be  administered  can  be  varied  accord- 
ing to  the  necessities  of  each  case.  It  is  seldom  necessary 
to  give  more  than  six  or  eight  ounces  of  brandy  in  twenty- 
four  hours,  yet  the  amount  required  is  to  be  determined  by 
the  frequency  and  character  of  the  pulse.  In  all  cases,  stim- 
ulants should  be  used  with  caution,  yet  when  the  necessity 
of  the  case  demands  it,  they  must  be  given  unsparingly ; 
especially  is  this  so  when  the  patient  has  been  addicted  to 
the  use  of  intoxicating  liquors.  The  period  immediately 
following  the  crisis  is  the  one  in  which  they  are  usually  most 
required  ;  symptoms  of  extreme  prostration  are  liable  to  oc- 
cur at  this  time,  especially  in  old  people.  In  pneumonia, 
affecting  the  young  and  vigorous,  stimulants  are  rarely 
called  for,  and  should  always  be  given  with  the  utmost 
caution. 

Narcotics,  even  in  cases  accompanied  by  great  restless- 
ness and  delirium,  must  be  cautiously  given,  especially  if 
there  be  any  evidences  of  cyanosis  ;  full  doses  often  increase 
the  prostration,  and  at  the  same  time  fail  to  produce  sleep. 
When  a  large  extent  of  lung-tissue  is  involved,  small  doses 
of  opium  sometimes  produce  the  most  complete  narcotism. 
If  the  pupils  are  contracted,  belladonna  should  be  given  in- 
stead of  opium.  As  I  have  already  stated,  if  the  pain  in 


150  TREATMENT. 

the  side  is  severe,  or  the  cough  harassing,  small  hypoder- 
mics of  morphine  will  be  found  of  service,  unless  the  other 
symptoms  centra-indicate  their  use  ;  small  doses  of  hydrate 
of  chloral  will  relieve  restlessness  and  procure  sleep,  in  some 
cases  where  opium  cannot  be  given  with  safety,  on  account 
of  the  loss  of  muscular  power  of  the  bronchi. 

Remedies  to  promote  expectoration  are  rarely  if  ever  of 
service  ;  accumulations  in  the  bronchi,  sufficient  to  occasion 
inconvenience,  are  due  to  a  loss  of  muscular  power,  for  the 
relief  of  which  expectorants  have  no  power — if  expectora- 
tion is  difficult  on  account  of  the  excessive  viscidity  of  the 
sputa,  alkalies  are  sometimes  of  service. 

Counter-irritants  in  the  early  stage  of  pneumonia  are  not 
only  useless,  but  greatly  increase  the  distress  of  the  patient. 
In  cases  where  there  is  considerable  pleuritic  effusion,  or 
when  resolution  is  delayed,  the  application  of  a  blister  over 
the  affected  side  is  sometimes  of  service.  When  the  evi- 
dences of  pulmonary  oedema  develop  in  the  unaffected  por- 
tion of  lung,  the  application  of  dry  cups  gives  most  marked 
relief. 

The  application  of  an  oil-silk  jacket  to  the  chest  has  come 
into  general  use  in  the  treatment  of  pneumonia.  There  is 
nothing  peculiar  or  specific  in  its  effect ;  if  it  acts  beneficially, 
it  does  so  by  protecting  the  surface  from  the  effect  of  sud- 
den changes  of  temperature.  The  use  of  carbonate  of  am- 
monia in  large  doses  has  recently  been  strongly  advocated 
as  a  heart-stimulant,  and  for  its  power  in  preventing  the 
formation  of  heart-clots  by  its  action  on  the  blood.  The 
local  action  on  the  stomach  of  large  doses  of  carbonate  of 
ammonia  is  that  of  an  irritant,  and  there  is  no  evidence  that 
its  remote  action  is  other  than  that  of  a  diffusible  stimulant ; 
in  this  respect  it  has  no  advantage  over  champagne,  while 
the  use  of  champagne  may  be  continued  much  longer  than 
the  ammonia  without  irritating  the  stomach. 

Great  care  should  be  taken  during  convalescence  from 
pneumonia,  that  the  nutrition  of  the  patient  is  maintained, 
and  that  the  surface  is  not  exposed  to  changes  of  tern  pera- 
ture.  Iron,  cod-liver  oil,  and  the  most  nutritious  diel  may 
be  freely  administered. 


PNEUMONIA.  151 

If  convalescence  is  slow,  and  three  or  four  weeks  after  the 
subsidence  of  the  acute  symptoms  the  patient  is  still  feeble, 
with  more  or  less  cough  and  expectoration,  a  change  of 
climate  and  of  habits  of  life  will  be  attended  with  most 
marked  beneficial  results. 

ACUTE  CATARRHAL  OR  BRONCHO-PNEUMONIA. 

I  will  now  pass  to  the  consideration  of  another  variety  of 
pneumonia,  which  in  its  acute  form  is  almost  exclusively 
confined  to  childhood  ;  while  the  chronic  form  furnishes  the 
anatomical  basis  of  almost  all  pulmonary  phthisis  ;  in  either 
case  it  is  a  secondary  affection.  It  differs  very  decidedly 
from  the  form  of  pneumonia  which  has  been  engaging  our 
attention,  both  in  its  clinical  and  pathological  history. 
\Vhile  croupous  pneumonia  usually  involves  an  entire  lobe 
of  a  lung,  catarrhal  is  limited  to  single  lobules  scattered 
more  or  less  abundantly  throughout  the  lung-substance,  in 
patches  varying  in  size  from  a  hemp-seed  to  an  egg,  or  even 
larger.  It  is  always  preceded  or  associated  with  inflamma- 
tion of  the  smaller  bronchi,  and  the  bronchi  which  lead  to 
the  consolidated  lobules  are  always  more  or  less  completely 
obstructed.  These  spots  of  consolidation  are  usually  found 
most  abundantly  in  the  posterior  and  anterior  portion  of 
the  lung. 

MORBID  ANATOMY. — In  a  lung  that  is  the  seat  of  acute 
lobular  pneumonia,  there  will  be  found  scattered  throughout 
its  substance,  small  red  or  yellowish  circumscribed  solid 
nodules,  which  do  not  inflate  when  the  lung  is  inflated  and 
are  not  granular  on  section.  If  they  are  situated  near  the 
surface  of  the  lung,  they  present  small  rounded  elevations  ; 
when  they  are  of  very  minute  size,  they  very  closely  resemble, 
and  not  unfrequently  are  mistaken  for  tubercle. 

When  the  nodules  are  of  considerable  size,  a  fluid  of  a 
reddish  or  grayish  color  can  be  made  to  ooze  from  their  cut 
surface ;  the  cut  surface  is  smooth,  and  not  granular  as  in 
croupous  pneumonia,  and  the  change  in  color  commences  at 
the  centre  of  the  consolidated  spot,  and  gradually  shades 
off  towards  the  circumference.  These  nodules  are  less  tough 
than  healthy  lung-tissue  and  break  down  easily  on  pres- 

Olr  3l=kT 

KS    k   b  UUUIEU 


152  MORBID   ANATOMY. 

sure ;  they  sink  to  the  bottom  of  the  vessel  when  thrown 
into  water.  This  form  of  pneumonia  runs  through  the  same 
stages  as  croupous  pneumonia,  viz. : 

first,  the  stage  of  engorgement. 

Second,  the  stage  of  red  hepatization. 

Third,  the  stage  of  gray  hepatization. 

The  stage  of  gray  hepatization  may  terminate  in  resolu- 
tion, purulent  infiltration,  or  cheesy  degeneration  ;  the  ten- 
dency to  pass  into  cheesy  degeneration  is  much  stronger 
in  catarrhal  than  in  croupous  pneumonia.  If  the  nodules 
have  reached  the  stage  of  gray  hepatization,  they  are  of 
a  grayish -yellow  color,  and  exceedingly  friable,  and  the  fluid 
that  flows  from  their  cut  surface  is  of  a  milky  consistency. 
The  small  bronchi  leading  to  the  hepatized  lobules  are 
usually  filled  with  tenacious  mucus  or  muco-pus,  their 
walls  are  more  or  less  thickened,  and  their  calibre  is 
enlarged, — peri-bronchitis  may  also  be  present. 

When  catarrhal  pneumonia  involves  a  large  portion  of 
lung,  perhaps  a  whole  lobe,  as  sometimes  happens,  its  gross 
appearance  closely  resembles  a  lobe  of  lung  which  is  the 
seat  of  croupous  pneumonia,  and  it  will  often  require  a 
careful  examination  to  draw  the  line  of  distinction  between 
the  two  conditions. 

By  observing  the  following  differences,  the  distinction 
may  always  be  made.  In  croupous  pneumonia,  the  in- 
flammatory process  uninterruptedly  advances  from  one 
point,  from  the  base  upward ;  while  in  catarrhal  pneumo- 
nia there  are  a  great  number  of  independent  centres  in  the 
consolidated  portion,  exhibiting  various  degrees  of  pro- 
gress, one  lobule  after  another  becoming  involved  in  the 
pneumonic  process.  Under  these  circumstances,  when  a 
section  of  the  consolidated  lung-tissue  is  made,  its  cut  sur- 
face presents  a  mottled  appearance,  which  is  due  to  the 
changes  in  color  presented  by  lobules  in  the  different  stages 
of  the  pneumonic  process, — lobules  in  the  first,  second,  and 
third  stages  will  be  found  scattered  irregularly  through  the 
consolidated  lobe.  These  two  varieties  of  pneumonia  also 
differ  in  the  character  of  the  exudation  which  takes  place 
into  the  air-cells  and  smaller  bronchi. 

-r>3JJOrj 

Z  K  f.\Cj\  £  7  K  T 


ACUTE   CATAKKHAL  PNEUMONIA.  153 

In  the  first  stage  of  catarrhal  pneumonia,  changes  similar 
to  those  already  described  as  occurring  in  the  congestive 
stage  of  croupous  pneumonia,  take  place  in  the  blood-ves- 
sels of  the  alveoli,  and  a  slight  amount  of  tenacious  exuda- 
tion is  poured  out  into  the  cavity  of  the  alveoli.  As  the 
pneumonic  process  reaches  the  stage  of  red  hepatization, 
the  alveoli  become  filled  with  a  solid  material,  which  differs 
very  essentially  from  the  exudation  in  the  second  stage  of 
croupous  pneumonia.  While  in  the  second  stage  of  croup- 
ous pneumonia  the  exudation  is  chiefly  made  up  of  fibril- 
lated  fibrin,  blood-globules,  lymphoid  cells,  and  a  small 
number  of  large  nucleated  cells, — in  catarrhal  pneumonia 
there  is  no  fibrillated  fibrin,  there  is  a  smaller  number  of 
lymphoid  cells,  few  red  blood-globules,  and  a  much  larger 
number  of  large  nucleated  cells  (changed  epithelial  cells) — 
if  any  fibrin  is  present  it  is  granular.  The  rapidity,  amount, 
and  character  of  the  cell-formation  determines  the  future  of 
the  pneumonia,  and  decides  whether  it  is  to  go  on  to  resolu- 
tion, purulent  infiltration,  or  cheesy  hepatization.  If  reso- 
lution or  purulent  infiltration  occur,  the  inflammatory  pro- 
ducts undergo  changes  similar  to  those  already  described  as 
taking  place  in  croupous  pneumonia.  If,  however,  the  cell- 
formation  is  abundant,  so  as  to  distend  the  alveoli,  the  exu- 
dation, instead  of  passing  through  the  stages  of  resolution, 
undergoes  fatty  and  afterward  cheesy  metamorphosis,  and 
we  have  cheesy  hepatization  or  chronic  catarrhal  pneumonia. 
The  inflammatory  products  which  obstruct  the  bronchi  lead- 
ing to  the  consolidated  lobules,  undergo  changes  similar  to 
those  that  take  place  in  the  air-cells,  and  are  removed  by 
absorption  and  expectoration  or  become  cheesy. 

Whenever  the  inflammatory  products  in  the  alveoli  or 
bronchi  become  cheesy,  months  are  required  for  the  comple- 
tion of  the  changes,  and  while  these  changes  are  taking 
place,  hyperplasia  of  the  connective-tissue  of  the  affected 
portion  of  lung  occurs,  and  as  a  result  of  this  connective- 
tissue  increase,  there  is  more  or  less  fibrous  induration  of 
the  lung.  This  last  condition  corresponds  to  the  anatomi- 
cal changes  of  catarrhal  phthisis  or  chronic  catarrhal  pneu- 
monia, and  will  be  more  fully  described  under  that  head. 


154  ETIOLOGY. 

If  lobules  on  the  surface  of  the  lung  become  involved, 
the  pleura  covering  them  also  becomes  involved,  and  under- 
goes the  same  changes  as  in  croupous  pneumonia. 

ETIOLOGY. — Closely  connected  with  the  morbid  anatomy 
of  acute  catarrhal  pneumonia  is  its  causation ;  it  is  essen- 
tially a  disease  of  childhood,  occurring  most  frequently 
between  one  and  six  years  of  age.  In  the  great  majority 
of  instances,  it  is  preceded  by  bronchitis,  being  either  the 
result  of  the  direct  extension  of  inflammation  from  the 
minute  bronchi  to  the  alveoli,  or  more  commonly  being  set  up 
in  collapsed  lobules.  It  may  occur  in  connection  with  he- 
morrhagic  or  pysemic  pulmonary  infarction.  That  form  of 
pneumonia  which  is  developed  in  lung-tissue  in  consequence 
of  obstructed  circulation,  whether  from  pressure  or  from 
interference  with  capillary  circulation,  is  almost  always 
catarrhal  in  character.  Pneumonias  in  connection  with 
pigment  induration  and  in  phthisis  are  usually  catarrhal. 

In  the  great  majority  of  cases,  this  form  of  pneumonia 
occurs  in  lungs  which  are  the  seat  of  pulmonary  collapse  ; 
a  bronchial  tube  becomes  obstructed,  collapse  of  the  air- 
vesicles  beyond  the  obstruction  takes  place,  and  following 
this  a  catarrlial  pneumonia.  When  the  collapse  of  a  lobule 
occurs,  the  pressure  upon  the  capillary  vessels  incident  to 
the  filling  of  the  air-cells  with  air  is  removed,  consequently 
the  walls  of  the  capillaries  become  distended  and  dilated, 
and  allow  of  an  increased  quantity  of  blood  in  the  col- 
lapsed lobule,  and  then,  in  accordance  with  a  well-estab- 
lished law,  a  rapid  cell-formation  takes  place  in  the  collapsed 
vesicles,  the  lobule  becomes  distended  to  its  normal  size,  and 
we  have  the  second  stage  of  catarrhal  pneumonia. 

This  is  usually  the  manner  in  which  acute  catarrhal  pneu- 
monia is  developed.  It  is  especially  liable  to  be  developed  in 
the  bronchitis  which  attends  whooping-cough,  measles, 
diphtheria  and  influenza.  Debility,  inhalation  of  impure 
air,  and  long-continued  recumbent  posture  predispose  to 
its  development.  Acute  pneumonia  occurring  in  the  aged 
and  in  enfeebled  adults,  and  in  those  suffering  from  acute 
or  chronic  disease,  is  frequently  catarrhal  in  its  nature. 


LECTURE    XIII. 


PNEUMONIA. 


Acute  Catarrhal  Pneumonia  (continued). — Interstitial  Pneumonia. 

A  T  my  last  lecture,  I  spoke  to  you  of  the  morbid  anatomy 
and  etiology  of  acute  catarrhal  pneumonia.  I  will  now  con- 
tinue the  history  of  this  affection,  by  inviting  your  attention 
to  its  symptoms. 

SYMPTOMS. — It  is  difficult  to  give  a  detailed  history  of  the 
phenomena  which  attend  the  development  of  this  affection, 
for  it  is  rarely  a  primary  disease,  and  its  symptoms  are 
always  more  or  less  obscured  by  those  of  the  diseases  by 
which  it  has  been  preceded.  When  it  occurs  as  an  acute 
affection,  the  phenomena  which  attend  its  development  very 
closely  resemble  those  of  croupous  pneumonia. 

Its  onset  is  usually  marked  by  a  slight  rigor  and  a  cer- 
tain elevation  of  temperature.  In  bronchitis,  the  tempera- 
ture rarely  reaches  102°  F. ;  on  the  development  of  acute  ca- 
tarrhal pneumonia  it  rises  in  a  few  hours  to  104°  F.,  or  even 
higher.  The  pulse  and  respiration  are  accelerated.  The 
respiration,  which  before  has  been  labored,  now  becomes 
rapid  and  panting.  The  countenance  becomes  flushed  and 
anxious,  the  nostrils  are  distended,  and  there  is  a  visible 
increased  action  of  the  thoracic  muscles,  accompanied  by 
great  restlessness.  The  cough,  which  previously  has  been 
loose  and  bronchial  in  character,  becomes  dry,  hacking  and 
painful,  and  the  countenance  during  the  paroxysms  of 
coughing  assumes  a  distressed  expression ;  the  expectora- 


156  SYMPTOMS. 

tion  is  scanty,  scarcely  ever  "rusty,"  and  in  very  young 
subjects  altogether  wanting. 

The  course  of  this  form  of  pneumonia  may  be  exceedingly 
acute  and  rapid,  or  it  may  be  subacute  in  character,  and 
run  a  slow,  lingering  course.  When  it  runs  an  acute  course, 
it  may  prove  fatal  in  a  few  days,  especially  in  feeble  chil- 
dren. In  such  cases,  the  mucous  surfaces  become  livid,  and 
the  patient  cyanotic.  The  restlessness  is  extreme,  dysp- 
noea becomes  severe,  the  patient  passes  into  a  stupid  or 
semi-comatose  condition,  the  respiration  becomes  more 
and  more  superficial  and  hurried,  and  convulsions  often 
terminate  the  case,  although  death  may  occur  by  slow 
asphyxia  and  exhaustion. 

The  subacute  form  often  occurs  in  the  bronchitis  of  stru- 
mous  children,  and  in  that  which  accompanies  measles  and 
whooping-cough.  Its  occurrence  is  marked  by  an  elevation 
of  temperature,  but  the  rise  is  not  as  great  or  as  sudden  as  in 
acute  cases ;  it  rises  gradually  until  it  reaches  103°  F.  or  104° 
F.  The  cough  becomes  more  severe  and  metallic  in  charac- 
ter, and  the  respiration  changes  from  the  labored  respira- 
tion of  bronchitis  to  the  rapid,  panting  respiration  of  pneu- 
monia. The  patient  begins  to  lose  flesh,  becomes  pale,  has  pro- 
fuse sweatings  and  tits  of  exhaustion  ;  the  appetite  becomes 
capricious  or  is  entirely  lost,  so  that  it  is  difficult  to  get  him 
to  take  food  ;  loss  of  strength  and  emaciation  are  progressive ; 
the  face  appears  bloated,  small  indolent  abscesses  appear  on 
nates  and  back,  the  patient  assumes  the  appearance  of  ex- 
treme anaemia,  and  finally  death  slowly  comes  from  wasting 
and  exhaustion.  Perhaps,  when  there  is  no  longer  any 
hope  of  recovery,  after  a  prolonged  illness,  resolution  of 
the  consolidated  lung  takes  place,  and  a  slow  though  com- 
plete recovery  is  reached. 

It  is  very  rare  for  rapid  resolution  to  take  place  in  any 
form  of  catarrhal  pneumonia,  and  when  it  does  occur,  there 
is  never  the  sudden  decline  of  temperature  so  characteristic 
of  croupous  pneumonia.  Catarrhal  pneumonias  are  more 
likely  than  croupous  to  be  subacute  or  chronic  in  character. 

The  two  varieties  of  acute  catarrhal  pneumonia  to  which 
I  have  referred  differ  in  severity  rather  than  in  type. 


ACUTE  CATAEEHAL   PNEUMONIA.  157 

PHYSICAL  SIGNS. — When  the  pneumonic  spots  are  small 
and  surrounded  by  normal  lung-tissue,  there  are  no  physi- 
cal evidences  of  their  existence. 

If,  however,  the  pneumonic  nodules  are  of  considerable 
size  and  are  situated  near  the  surface  of  the  lung,  there  will 
be  localized  dulness  on  slight  percussion,  especially  along 
the  posterior  and  anterior  border  of  the  lungs,  more  particu- 
larly over  that  portion  which  covers  the  heart ;  this  dulness 
will  not  change  by  coughing,  nor  be  found  changed  at  dif- 
ferent examinations.  Increased  vocal  resonance  and  fremi- 
tus  over  the  part  affected  will  also  be  present. 

On  auscultation,  the  respiratory  murmur  may  be  feeble 
at  certain  points  over  the  surface  of  the  lung,  which  simply 
tells  of  obstructed  bronchial  tubes  ;  but  over  the  points  of 
localized  dulness  the  breathing  will  assume  a  bronchial 
character,,  and  if,  while  you  are  carefully  listening  at  these 
points,  the  patient  is  directed  to  cough  violently  or  is  made 
to  cry,  at  the  end  of  the  inspiration  that  follows  the  cough- 
ing or  crying,  yon  will  hear  tine  crackling  rales  of  a  metallic 
character. 

Acute  catarrhal  pneumonia,  involving  a  large  extent  of 
lung  (as,  for  instance,  a  whole  lobe)  cannot  be  distinguished 
by  its  physical  signs  from  croupous  pneumonia. 

DIFFERENTIAL  DIAGNOSIS. — It  is  always  difficult,  and 
sometimes  impossible,  in  the  early  stage  of  acute  catarrhal 
pneumonia,  to  distinguish  it  from  capillary  bronchitis ;  the 
most  reliable  element  of  distinction  in  the  differential  diag- 
nosis is  the  sudden  rise  in  temperature  which  marks  the 
onset  of  the  pneumonic  process. 

It  is  also  difficult  to  distinguish  it  from  collapse  of  the 
lung,  especially  as  the  two  conditions  often  exist  in  the 
same  lung.  Here  also  the  temperature  is  all-important  as  an 
element  of  diagnosis,  for  pulmonary  collapse  will  not  be  at- 
tended by  elevation  of  temperature,  which  is  so  constant  an 
attendant  of  pneumonia.  It  is  also  sometimes  difficult  to 
determine  whether  a  given  case  of  pneumonia  is  croupous  or 
catarrhal  in  its  nature.  The  points  of  diiferential  diagnosis 
are  the  following,  viz.  :  acute  catarrhal  pneumonia  is  almost 
always  preceded  by  bronchitis,  while  croupous  pneumonia 


158  PKOGtfOSIS. 

is  rarely  preceded  by  bronchitis.  Catarrhal  pneumonia 
usually  affects  both  lungs  ;  croupous  is  usually  confined  to 
one.  Catarrhal  pneumonia  has  no  critical  days,  while  in 
croupous  a  day  of  crisis  is  the  rule.  Croupous  pneumonia 
has  its  characteristic  expectoration  ;  rusty  expectoration  is 
rare  in  catarrhal.  Croupous  pneumonia  is  ushered  in  by  a 
distinct  chill ;  in  catarrhal,  distinct  chills  rarely  occur.  There 
are  other  distinctions  between  these  two  affections,  but  these 
usually  will  be  sufficient  for  a  differential  diagnosis. 

It  is  far  more  difficult  to  distinguish  acute  catarrhal  pneu- 
monia from  acute  tuberculosis  than  from  any  other  dis- 
eased condition  of  the  lungs.  In  both  diseases  high  temper- 
ature is  the  leading  and  characteristic  feature.  Usually, 
however,  the  temperature  is  higher  in  acute  tuberculosis 
than  in  pneumonia,  yet  the  two  diseases  may  so  closely  re- 
semble one  another  as  to  render  a  differential  diagnosis  im- 
possible. In  most  cases,  if  not  in  all,  it  is  only  to  be  deter- 
mined by  the  history  of  the  case,  and  such  assistance  as 
may  be  derived  from  the  evidences  that  tubercles  are  present 
in  other  organs  of  the  body.  There  is  one  fact  that  may  be 
of  essential  service  under  such  circumstances,  and  that  is, 
that  the  bronchitis  which  may  be  present  precedes  the  pneu- 
monia, and  follows  the  development  of  acute  tuberculosis. 

PROGNOSIS. — The  prognosis  in  acute  catarrhal  pneumonia 
depends  almost  entirely  upon  the  circumstances  which  at- 
tend its  development,  and  upon  the  activity  of  its  processes. 

The  prognosis  is  better  when  it  occurs  with  measles,  than 
when  it  occurs  with  whooping-cough.  It  is  better  in  chil- 
dren who  are  well-nourished  and  vigorous  at  the  time  of  the 
attack,  than  in  those  who  are  debilitated  and  weakly. 

It  is  better  characterized  by  a  sudden  rise  in  temperature 
in  the  acute  form  of  the  disease,  than  when  it  is  subacute 
and  comes  on  more  gradually,  and  is  slower  in  its  progress. 
The  prognosis  is  better  in  one  who  has  no  organic  disease 
at  the  time  of  attack  than  in  one  who  is  already  suffering 
from  chronic  disease,  especially  of  the  lungs. 

Acute  catarrhal  pneumonia,  following  scarlatina  or  affec- 
tions of  the  kidney,  is  especially  dangerous.  Prognosis  is 
also  affected  by  the  hygienic  influences  which  surround 


PNEUMONIA.  159 

the  patient ;  anti-hygienic  surroundings  are  unfavorable  to 
recovery.  Whenever  the  attending  bronchitis  is  extensive, 
involving  a  large  portion  of  the  capillary  bronchi,  the  oc- 
currence of  lobular  pneumonia  renders  the  prognosis  un- 
favorable. 

Among  the  symptoms  which  may  be  regarded  as  unfavor- 
able is  a  temperature  exceeding  1058  F.  ;  increasing  cya- 
nosis and  diminished  power  of  cough  and  expectoration,  as 
shown  by  rales  in  the  trachea  and  large  bronchi  ;  to  these 
may  be  added  extreme  frequency  and  feebleness  of  the 
pulse,  somnolency,  coma,  and  convulsions. 

That  form  of  acute  catarrhal  pneumonia  which  occurs  in 
connection  with  pyaemia  is  extremely  dangerous,  for  the 
reason  that  rapid  suppuration  almost  certainly  follows  its 
development.  When  developed  in  connection  with  hemor- 
rhagic  infarctions  the  prognosis  is  not  as  unfavorable  as 
when  it  occurs  with  pysemic  infarctions. 

TREATMENT. — In  the  treatment  of  this  form  of  pneu- 
monia, you  must  constantly  bear  in  mind  the  fact  that  in 
almost  all  cases  it  is  a  secondary  disease,  and  that  its  oc- 
currence indicates  that  the  patient  is  in  an  enfeebled  con- 
dition. 

It  is  of  primary  importance  for  the  successful  manage- 
ment of  the  disease  that  the  patient  be  kept  in  an  equable 
temperature.  The  apartment  occupied  by  the  patient 
should  be  large,  well-ventilated,  and  kept  at  a  temperature 
ranging  between  65°  F.  and  70°  F. ;  no  sudden  variations  in 
temperature  must  be  allowed,  and  yet  thorough  ventilation 
is  absolutely  necessary.  The  body  should  be  covered  with 
flannel,  and  the  patient  kept  in  bed  until  convalescence  is 
fully  established. 

All  so-called  antiphlogistic  measures  or  depressing  reme 
dies  must  be  avoided  ;  that  which  is  most  to  be  dreaded  in 
this  disease  is  debility,  and  nothing  should  be  done  in  the 
way  of  treatment  which  will  contribute  to  produce  this 
effect.  Even  when  the  disease  assumes  a  very  active  form, 
depletion  is  not  allowable  ;  blood-letting,  antimony,  calomel, 
and  veratrum  are  all  contra-indicated. 

As  a  rule,  stimulants  must  be  commenced  at  the  very 


160  TEEATMEXT. 

onset  of  the  disease,  and  their  use  continued  throughout 
its  entire  course  ;  the  quantity  of  stimulants  to  be  adminis- 
tered to  be  determined  by  the  necessities  of  each  case. 

Here  again,  as  in  croupous  pneumonia,  the  Germans  re- 
commend the  application  of  cold  compresses  to  the  chest, 
and  here  also  my  experience  has  been  altogether  against 
cold  applications,  for  the  great  risk  of  sudden  change  of 
temperature  which  attends  their  application  almost  neces- 
sarily contra-indicates  their  use.  As  regards  the  applica- 
tion of  counter-irritants  to  the  chest,  all  kinds  have  seemed 
to  me  to  do  more  harm  than  good.  I  am  certain  that  blis- 
ters should  never  be  applied  to  the  chest  of  young  children 
suffering  from  catarrhal  pneumonia.  Dry  cups  are  admis- 
sible, and  they  should  be  used,  if  counter-irritation  is  to  be 
employed. 

In  this  form  of  pneumonia  the  important  things  to  be  ac- 
complished, are  the  reduction  of  temperature,  and  the  arrest 
of  cell-development.  The  remedy  which  I  believe  has 
power  to  accomplish  both  of  these  results  is  the  sulphate 
of  quinine.  It  may  be  given  in  full  doses,  both  during  the 
period  of  fever,  and  as  an  aid  to  resolution ;  the  benefit  de- 
rived from  its  administration  is  most  marked  during  the 
active  stage  of  the  disease.  From  ten  to  twenty  grains  may 
be  administered  daily  to  a  child  three  years  of  age. 

If  the  attending  bronchitis  is  extensive,  it  should  be  re- 
lieved as  far  as  possible  by  vapor  inhalations,  and  the  free 
internal  use  of  muriate  of  ammonia,  according  to  the  plan 
already  proposed  for  the  treatment  of  capillary  bronchitis 
in  children. 

If  the  child  has  been  ill  two  or  three  weeks,  and  begins  to 
show  the  emaciation  which  is  so  frequently  present  in  the 
subacute  form  of  the  disease,  cod-liver  oil  will  be  found  of 
great  service.  The  administration  of  this  remedy  will  be 
found  much  more  beneficial  in  children  than  in  adults.  It 
should  be  administered  in  combination  with  the  phosphate 
of  lime  and  soda,  and  should  be  given  in  as  large  quantities 
as  possible,  without  offending  the  stomach. 

If  the  patient  is  anaemic,  some  preparation  of  iron  will  be 
of  service  ;  iron  reduced  by  hydrogen  is  far  more  serviceable 


ACUTE   CATARRIIAL   PNEUMONIA.  161 

than  the  syrup  of  the  iodide  of  iron,  which  is  so  commonly 
employed.  At  the  end  of  six  weeks  or  two  months  the 
question  of  a  change  of  climate  may  be  presented  ;  this  not 
unfrequently  proves  very  beneficial,  and  children  often  will 
give  evidence  of  rapid  improvement  within  a  few  days  after 
the  change  has  been  made. 

During  the  entire  course  of  the  disease  the  food  should 
be  fluid,  nutritious,  and  given  in  the  most  concentrated 
form. 

Convalescence  should  be  managed  with  the  greatest  care, 
so  as  to  avoid  fatigue  and  exposure,  which  may  bring  on  a 
fresh  bronchial  catarrh. 

INTERSTITIAL  PNEUMONIA. 

The  next  form  of  pneumonia  which  will  engage  our  atten- 
tion is  known  as  interstitial  or  fibrous  pneumonia;  some 
writers  have  called  this  form  chronic  pneumonia,  but  this 
term  is  apt  to  lead  to  confusion. 

It  is  rarely,  if  ever,  a  primary  affection  ;  in  this  respect  it 
resembles  catarrhal  pneumonia,  but  it  differs  from  it  in  the 
primary  seat  of  the  inflammatory  changes. 

MORBID  ANATOMY. — The  first  change  that  is  noticed  in  a 
lung  that  is  the  seat  of  fibrous  pneumonia,  is  hypersemia 
and  swelling  of  the  .intercellular  and  interlobular  tissue, 
and  proliferation  of  the  alveolar  epithelium.  This  change  is 
very  soon  followed  by  a  more  or  less  rapid  hyperplasia  of 
the  connective-tissue ;  a  large  number  of  cells  are  developed 
in  the  connective-tissue,  which  very  soon  assume  the  char- 
acteristic shape  and  appearance  of  connective-tissue  cells, 
which  will  be  seen  overlapping  and  interlacing  each  other 
to  a  greater  or  less  extent  all  through  the  intercellular  and 
interlobular  structure  of  the  affected  portion  of  the  lung. 

At  first  the  tissue  is  soft,  and  contains  more  or  less  blood  ; 
but  like  all  other  connective-tissue  formations,  it  very  soon 
becomes  firm ;  after  a  time,  it  contains  little  blood,  and 
looks  like  a  callous,  indurated  texture,  having  all  the  ap- 
pearance of  fully-developed  connective-tissue. 

The  interstitial- tissue  is  not  only  increased,  but  in  conse- 
quence of  its  increase,  the  calibre  of  the  air-cells  is  markedly 
11 


162  MORBID   ANATOMY. 

diminished.  The  development  of  this  new  connective-tissue 
may  reach  such  an  extent,  that  all  of  the  air-cells  in  that 
portion  of  the  ]  ung  which  is  the  seat  of  the  process  may  be 
destroyed,  and  no  trace  of  lung- tissue  left. 

With  two  exceptions,  this  process  always  commences 
with,  or  is  preceded  by,  lobular  pneumonia,  which  is  at- 
tended by  changes  in  the  epithelial  cells  of  the  alveoli ;  how 
far  these  exceptions  extend  is  not  quite  certain. 

It  is  undoubtedly  true  that  the  inflammatory  process 
which  gives  rise  to  pleuritic  thickenings  may  extend  into 
the  lung-substance  and  cause  the  formation  of  bands  of 
white  fibrous  tissue  more  or  less  extensively  throughout 
the  lung-substance,  and  thus  give  rise  to  quite  extensive 
fibrous  pneumonia. 

The  same  kind  of  a  process  may  also  commence  in  the 
connective-tissue  around  the  bronchi  and  blood-vessels  as 
well  as  in  the  walls  of  the  alveoli,  and  gradually  increase 
until  the  pulmonary  tissue  is  almost  entirely  lost  in  a  fibrous 
mass.  With  these  exceptions,  interstitial  pneumonia  is 
found  associated  either  with  lobular  or  lobar  pneumonia. 

A  lung  which  is  the  seat  of  fully-developed  fibrous  pneu- 
monia is  much  firmer  than  normal  lung-tissue,  is  solid  and 
hard  to  the  touch  ;  when  cut,  it  presents  a  smooth  shining 
appearance,  and  gives  a  creaking  sound  under  the  knife. 
It  varies  in  color, — at  one  time,  it  presents  a  white,  shining 
appearance, — at  another  time,  it  is  of  a  dark  slate  or  black 
color,  according  to  the  amount  of  pigmentation  which  it 
has  undergone.  In  some  cases,  the  development  of  fibrous 
tissue  will  only  be  manifested  by  lines  or  fibres  of  indura- 
tion running  through  the  lung ;  in  other  cases,  fibrous 
nodules  will  be  scattered  through  the  lung  in  such  num- 
bers that  almost  the  entire  lung  becomes  changed  into 
fibrous  tissue,  in  which  all  traces  of  air-cells  have  been 
obliterated. 

In  this  way,  the  apex  of  a  lung  may  be  changed  into  a 
firm  mass,  traversed  by  dense  bands  of  fibrous  tissue  (a 
peculiar  feature  of  this  disease  is,  that  it  is  usually  limited 
to  one  lung). 

The  bronchi  in  lung-tissue,  which  is  the  seat  of  fibrous 


INTERSTITIAL   PNEUMONIA.  163 

» 

pneumonia,  undergo  a  variety  of  changes.  As  a  rule,  they 
become  more  or  less  dilated.  How  these  dilatations  origi- 
nate, is  a  question  which  has  given  rise  to  much  discussion, 
and  it  is  by  no  means  clearly  settled  at  the  present  time. 

There  are  those  who  maintain  that  these  dilatations  are  con- 
sequent upon  the  retractions  incident  to  fibrous  induration. 
In  other  words,  when  a  lung  becomes  the  seat  of  fibrous 
pneumonia,  the  new  connective- tissue  contracts  in  obedience 
to  the  laws  which  govern  all  new  connective-tissue  forma- 
tions, and,  consequently,  the  lung  becomes  diminished  in 
size  ;  with  this  diminution  in  the  size  of  the  lung  comes  re- 
traction of  the  chest- walls  to  compensate  for  the  loss  of 
lung-tissue ;  but  this  compensation  has  a  limit,  and  does 
not  entirely  fill  the  vacuum  produced  by  the  diminished 
size  of  the  lung ;  consequently,  dilatation  of  the  bronchi 
takes  place  to  fill  the  deficiency.  It  seems  to  me  that  these 
retractions  of  the  new  fibrous  tissue  in  the  lung  would 
diminish  the  calibre  of  the  bronchial  tubes,  rather  than  in- 
crease their  size.  I  doubt  if  bronchial  dilatation  occurs  in 
lungs  which  are  the  seat  of  fibrous  pneumonia  unless  the 
pneumonia  has  been  preceded  by  more  or  less  extensive 
peri-bronchitis.  As  a  result  of  which  the  walls  of  the 
bronchial  tubes  become  weakened,  and  lose  their  elastic 
power  to  a  greater  or  less  extent.  Under  these  circum- 
stances, the  new  connective  development  subjects  at  dif- 
ferent points  these  weakened  tubes  to  constriction,  and,  as 
a  consequence  of  these  constrictions,  dilatations  are  formed. 
The  dilating  process  is  also  assisted  by  the  forced  inspira- 
tions which  always  attend  violent  coughing,  and  violent 
coughing  is  one  of  the  invariable  attendants  of  this  con- 
dition of  lung.  This  constitutes  the  condition  of  lung 
which  has  received  the  name  of  broncMectasis. 

Whenever,  in  a  portion  of  lung  that  is  the  seat  of  croupous 
or  catarrhal  pneumonia,  the  process  of  resolution  takes 
place  slowly,  connective-tissue  increase  is  very  apt  to  be 
established  and  interstitial  pneumonia  to  be  developed  in 
the  consolidated  lung-tissue.  Ordinarily,  resolution  in 
croupous  and  catarrhal  pneumonia  is  so  rapid  that  no 
permanent  change  takes  place  in  the  intervesicular  con- 


1 64  ETIOLOGY. 

nective-tissue  ;  but  when  it  is  delayed,  and  cheesy  degenera- 
tion of  the  inflammator}'  products  in  the  alveoli  and  bronchi 
occurs,  it  may  be  regarded  as  certain  that  more  or  less  exten- 
sive interstitial  pneumonia  is  taking  place. 

ETIOLOGY. — The  diseases  of  the  lungs  and  bronchi  which 
have  already  been  referred  to  as  favoring  the  development 
of  interstitial  pneumonia  may  be  ranked  among  its  causes. 

Encapsulated  abscesses,  or  infarctions  formed  in  the  lungs 
from  any  cause,  are  attended  and  followed  by  the  develop- 
ment of  interstitial  pneumonia  in  the  surrounding  lung-tis- 
sue, and,  consequently,  must  be  regarded  as  causes  of  its 
development. 

There  can  be  little  doubt  but  that  in  the  majority  of  cases 
this  disease  is  secondary  to  some  previous  pulmonary  affec- 
tion ;  consequently,  all  those  conditions  of  the  lung  which 
are  embraced  under  the  head  of  pulmonary  phthisis  are 
succeeded  by,  or  associated  with,  fibrous  pneumonia,  and 
therefore  may  be  regarded  as  causes  of  this  pathological 
condition. 

Some  writers  mention  it  as  a  primary  affection,  but  its 
occurrence  as  such  is  quite  doubtful. 

SYMPTOMS. — The  symptoms  which  attend  the  develop- 
ment of  interstitial  pneumonia  are  by  no  means  distinct. 
In  the  early  stage,  while  the  new  connective-tissue  forma- 
tions are  soft,  both  rational  and  physical  signs  are  indefinite. 

Clinical  experience  has  shown  that  if  croupous  pneu- 
monia passes  a  certain  period  and  the  dulness  on  percussion 
continues,  accompanied  by  bronchial  respiration  or  a  loss 
of  vesicular  breathing,  with  some  retraction  of  the  chest- 
walls,  fibrous  pneumonia  is  being  developed.  The  same 
inference  may  be  made  in  connection  with  catarrhal  pneu- 
monia, as  well  as  the  other  diseased  processes  already 
referred  to  in  connection  with  the  morbid  anatomy  of  the 
disease.  There  is  no  rise  in  temperature  or  change  in  the 
condition  of  the  pulse  indicating  its  occurrence.  The  first 
sign  which  positively  indicates  its  existence  is  retraction 
of  the  chest-wall  over  the  affected  portion  of  lung, — this 
retraction  becomes  more  and  more  marked  as  the  fibrous 
induration  increases.  With  the  retraction  there  are  drag- 


INTERSTITIAL   PNEUMONIA.  165 

ging  pains  in  the  affected  side,  and  a  cough  which,  when  the 
bronchi  are  dilated,  comes  on  in  severe  paroxysms  followed 
by  profuse  expectoration  ;  when  there  is  little  or  no  dilata- 
tion of  the  bronchi  the  expectoration  is  not  very  abundant ; 
sometimes  it  is  exceedingly  fetid  and  contains  caseous 
particles. 

Dyspnoea,  though  a  constant  attendant,  is  usually  not 
severe,  even  in  the  advanced  stages  of  the  disease  ;  so  long 
as  the  patient  is  quiet,  he  suffers  little.  He  habitually  lies 
on  the  affected  side ;  attempts  to  lie  on  the  other  increase 
the  dyspnoea  and  bring  on  the  cough. 

The  constitutional  symptoms  are  a  gradual  loss  of  flesh 
and  strength,  increasing  anaemia,  sometimes  night-sweats ; 
usually,  however,  there  is  no  fever.  The  development  of 
interstitial  pneumonia  is  attended  by  changes  in  the  heart 
which  indicate  obstructed  pulmonary  circulation. 

PHYSICAL  SIGNS. — After  retraction  of  the  lung  has  oc- 
curred, the  physical  evidences  of  interstitial  pneumonia  are 
distinct  and  easily  appreciated.  Inspection  will  show  re- 
traction of  the  chest-walls  over  the  affected  portion  of 
lung  with  marked  loss  of  expansive  movements  on  the 
affected  side.  Vocal  fremitus  is  usually  increased  ;  it  may 
be  diminished. 

On  percussion  the  sound  will  be  duller  than  in  croupous 
or  catarrhal  pneumonia,  or  it  will  have  a  hard,  wooden 
quality  ;  occasionally  over  large  bronchial  dilatations  there 
will  be  "cracked-pot  resonance." 

On  auscultation  over  the  affected  portion  of  lung,  the 
respiratory  murmur  is  either  feeble  and  absent,  or  heard 
only  over  limited  areas  ;  or  it  is  bronchial  in  character.  If 
bronchial  dilatation  exist,  you  may  have  cavernous  or  am- 
phoric respiration ;  often  after  coughing,  amphoric  respir- 
ation is  heard  where  it  was  absent  previous  to  the  cough. 
Mucous  rales  of  large  and  small  size  are  heard,  having  a 
sharp  metallic  quality  ;  if  bronchial  dilatations  contain 
fluid,  gurgles  of  large  size  will  be  heard. 

The  heart  is  often  displaced  toward  the  affected  side, 
the  amount  of  displacement  depends  upon  the  amount  of 
lung- shrinking  ;  it  is  usually  more  marked  when  the  disease 


166  DIFFERENTIAL  DIAGNOSIS. 

involves  the  right  lung ;  sometimes  the  liver  is  displaced 
upward. 

DIFFERENTIAL  DIAGNOSIS. — There  are  three  conditions 
that  are  liable  to  be  mistaken  for  fibrous  pneumonia.  These 
conditions  are  pleurisy  with  effusion,  pleurisy  with  re- 
traction, and  cancer  of  the  lung. 

First,  with  regard  to  pleurisy  with  effusion.  If  the  pleu- 
ral  cavity  is  distended  with  fluid,  bulging  of  the  intercostal 
spaces  will  be  present.  In  fibrous  pneumonia  there  will  be 
retraction  over  that  portion  of  the  lung  which  is  the  seat  of 
the  induration.  In  pleurisy  with  effusion,  the  percussion- 
sound  over  the  surface  of  the  fluid  is  flat,  while  in  fibrous 
pneumonia  it  is  wooden  in  character.  To  the  accustomed 
ear  the  difference  in  the  percussion-sound  excludes  or 
establishes  the  existence  of  pleuritic  effusion  ;  besides,  in 
most  cases  of  pleurisy  a  change  in  the  position  of  the 
patient  will  change  the  line  of  dulness.  If,  however,  doubts 
still  exist,  the  introduction  of  the  exploring  trocar  will 
settle  the  question. 

Bronchial  respiration  may  be  present  in  both  instances, 
but  it  will  be  more  diffused  in  pleurisy,  and  generally  can 
be  heard  most  distinctly  near  the  root  of  the  lungs  at  the 
lower  border  of  the  scapula  ;  whereas,  in  fibrous  induration, 
the  bronchial  respiration  will  be  most  marked  at  the  point 
where  the  induration  is  most  intense. 

There  is  frequently  great  difficulty  in  distinguishing 
fibrous  pneumonia  from  pleurisy  with  retraction,  and  with- 
out the  aid  of  an  intelligent  history  it  is  often  impossible. 
There  will  be  retraction  of  the  chest- walls  and  dulness  upon 
percussion  alike  in  character  in  both. 

The  presence  of  bronchial  respiration  is  usually  well- 
marked  in  fibrous  induration,  while  in  pleurisy  with  retrac- 
tion the  respiratory  sounds  are  feeble  or  entirely  absent  over 
the  affected  side.  Besides,  the  shrinking  which  usually 
attends  the  pleurisy  causes  actual  deformity  of  the  chest ; 
while  that  which  is  seen  in  connection  with  the  pneumonia 
is  uniform  and  produces  simply  a  diminution  in  the  size  of 
the  affected  side. 

In   distinguishing  fibrous  induration  of  the  lung  from 


INTEKSTITIAL   PNEUMONIA.  167 

cancer  of  the  lung,  although  the  physical  signs  of  the  two 
conditions  are  very  similar,  the  history  of  the  two  diseases 
is  so  different  that  by  that  alone  a  differential  diagnosis 
can  be  made. 

Then,  the  existence  or  non-existence  of  cancer  in  other 
parts  of  the  body  is  important,  for  primary  cancer  of  the 
lung  or  pleura  is  rarely  met.  After  the  cancer  has  become 
sufficiently  extensive  to  assimilate  the  appearance  of  pneu- 
monia, there  can  be  but  very  little  difficulty  in  diagnosis  ; 
for  at  that  late  period  the  constitutional  disturbance 
attending  development  of  cancer,  as  manifested  by  the 
cachectic  look  and  the  glandular  enlargements,  will  make 
the  way  to  a  correct  diagnosis  quite  plain. 

PKOGNOSIS. — The  prognosis,  as  regards  time,  in  inter- 
stitial pneumonia  is  good.  Persons  with  this  disease  live 
for  many  years,  and  only  suffer  from  the  dyspnoea  incident 
to  a  diminution  of  serviceable  lung-tissue.  As  it  is  rarely, 
if  ever,  an  independent  affection,  the  prognosis  will  depend 
to  a  very  great  extent  upon  the  original  disease.  Exten- 
sive induration  of  the  lung,  following  a  slowly  resolving 
croupous  pneumonia,  and  accompanying  a  chronic  bron- 
chitis, may  exist  for  a  long  time  after  bronchial  dilatations 
have  formed.  Under  these  circumstances  there  is  danger 
that  the  heart  or  kidneys  will  become  secondarily  involved 
and  death  ensue  from  general  dropsy,  as  a  result  of  the 
disturbance  of  the  general  circulation.  Patients  suffering 
in  this  way  are  liable  to  attacks  of  exhausting  diarrhoea. 
Occasionally  death  is  the  result  of  hemorrhage. 

Whatever  intercurrent  disease  may  occur  in  one  who  is 
the  subject  of  chronic  interstitial  pneumonia,  it  will  have  a 
direct  influence  on  the  question  of  prognosis. 

TEEATMEISTT. — Fully-developed  interstitial  pneumonia  is 
incurable, — cicatricial  tissue  formed  in  the  lungs  remains 
during  the  life  of  the  patient ;  something  perhaps  may  be 
done  to  arrest  its  further  development.  If  it  is  developed 
from  a  bronchitis,  it  is  very  important  to  guard  against  the 
recurrence  of  the  bronchitis.  As  we  are  powerless  to  effect 
the  closure  of  any  dilated  bronchus  that  may  exist,  we 
must,  by  stimulating  inhalation,  endeavor  to  rid  these  dila- 


168  TKEATMENT. 

tations  of  accumulated  secretion  and  thus  prevent  fetid 
accumulation  which  shall  to  a  greater  or  less  extent 
endanger  the  adjacent  lung-tissue. 

The  inhalation  of  benzoin  or  oil  of  turpentine  will  best 
accomplish  this  result. 

This  form  of  pneumonia  will  be  more  fully  considered 
under  the  head  of  pulmonary  phthisis. 


LECTURE    XIV. 


PLEURISY. 

Definition. — Varieties.  — Acute  Pleurisy. 

Tins  morning  I  come  to  the  study  of  those  changes 
which  take  place  in  the  pleura  as  the  result  of  disease. 
Diseased  processes  affecting  the  pleura  and  the  pulmonary 
tissue  are  often  intimately  associated,  and  for  this  reason 
diseases  of  the  pleura  may  properly  be  considered  in  con- 
nection with  diseases  of  the  lungs.  It  is  not  necessary  for 
me  to  describe  the  anatomical  arrangement  of  this  very 
extensive  serous  membrane,  for  that  has  already  been  done 
by  one  of  my  colleagues  ;  I  shall  therefore  at  once  enter 
upon  the  history  of  its  diseases. 

By  the  term  pleurisy  is  understood  either  a  partial  or 
general  inflammation  of  one  or  both  pleura. 

This  inflammation  may  run  an  acute,  subacute,  or  chron- 
ic course,  and  it  may  be  attended  by  a  serous,  fibrous,  or 
cellular  exudation.  The  serous  exudation  gravitates  to  the 
most  dependent  portion  of  the  pleural  sac ;  the  fibrinous 
exudation  is  spread  over  the  free  surface  of  the  pleura,  and 
the  cells  are  entangled  in  the  meshes  of  the  fibrine  or  are 
contained  in  the  serous  effusion. 

I  shall  describe  pleurisy  under  four  heads  : — 

First,  ACUTE  PLEURISY. 

Second,  SUBACUTE  PLEURISY. 

TJiird,  CHRONIC  PLEURISY,  or  EMPYEMA. 

Fourth,  HYDROPJSTEUMOTIIORAX. 


170  MORBID   ANATOMY. 

In  the  first,  or  acute  form  the  symptoms  are  always  well- 
defined,  the  course  rapid,  and  the  exudation  principally 
fibrinous. 

In  the  second,  or  subacute  form  the  symptoms  are  mild, 
the  disease  slow  in  its  development,  and  the  exudation 
chiefly  serum. 

The  third  form,  or  chronic  pleurisy,  occurs  in  persons  of 
debilitated  constitutions  ;  usually  it  is  slow  in  its  develop- 
ment, and  the  exudation  is  always  sero-purulent. 

The  fourth  form,  or  hydropneumothorax,  is  a  modified 
form  of  chronic  pleurisy,  with  perforation  of  the  lung,  which 
admits  air  into  the  pleural  cavity. 

Pleurisy  may  occur  as  a  primary  or  as  a  secondary  disease. 

Primary  pleurisies  are  those  which  occur  as  the  result  of 
the  direct  action  of  the  irritant  upon  the  pleural  membrane. 

Secondary  pleurisies  are  those  in  which  the  pleural  in- 
flammation is  secondary  to  some  other  visceral  disease  or  to 
some  constitutional  disorder,  such  as  pyaemia,  septicaemia, 
typhus,  and  typhoid  fever,  etc.  This  variety  of  pleurisy  is 
especially  liable  to  be  developed  in  connection  with  pulmo- 
nary diseases.  It  is  a  well-established  fact  that  when  a  pul- 
monary inflammation  reaches  the  surface  of  the  lung, 
pleuritic  inflammation  will  be  developed,  at  least  in  that 
portion  of  the  pleura  which  immediately  covers  the  dis- 
eased pulmonary  tissue. 

ACUTE  PLEURISY. 

MORBID  ANATOMY. — The  first  apparent  anatomical  change 
in  this  form  of  pleurisy  is  a  reddening  of  the  pleural  mem- 
brane from  hypersemia  of  the  capillaries  of  the  serous  and 
subserous  connective  tissue  ;  sometimes  this  reddening  occurs 
as  little  spots  of  ecchymosis.  Following  this,  you  will  find 
the  membrane  losing  its  natural  lustre ;  this  is  due  to  the 
detachment  of  its  epithelial  covering ;  the  pleural  tissue  is 
infiltrated,  and  presents  a  somewhat  swollen  appearance  ; 
gradually  its  free  surface  begins  to  assume  a  rough  shaggy 
appearance  ;  this  is  due  to  an  exudation  upon  its  surface  of 
a  soft,  red,  elastic  material,  which  may  be  spread  over  the 
entire  surface  of  the  pleura,  or  occur  in  patches ;  it  may  be 


ACUTE   PLEURISY.  171 

sufficient  to  agglutinate  the  two  pleural  surfaces.  This  elas- 
tic substance  is  coagulable  lymph  (fibrin),  which  is  poured 
out  from  the  walls  of  the  vessels  and  collects  upon  the  free 
surface  of  the  pleura  ;  it  encloses  in  its  meshes  an  innumer- 
able number  of  young  cells,  which  are  either  changed  epi- 
thelial cells,  or  wandering  globules  that  have  migrated  from 
the  walls  of  the  blood-vessels. 

If  serous  effusion  occurs,  the  lymph  exudation  is  sus- 
pended in  it,  in  the  form  of  ragged  flakes ;  this  fluid  will 
also  be  found  to  contain  cells  or  free  nuclei.  In  this  form 
of  pleurisy,  there  is  usually  very  little  serous  effusion, 
while  the  plastic  material  is  abundant.  In  very  recent  pleu- 
ritic inflammation,  as  you  remove  the  plastic  exudation 
from  the  surface  of  the  pleura,  you  will  find  immediately 
underneath  it  a  layer  of  embryonic  cells  in  a  condition  to 
develop  into  new  connective  tissue.  It  would,  therefore,  ap- 
pear that  usually,  as  soon  as  the  serous  surface  is  denuded 
of  its  epithelium,  a  layer  of  new  cells  are  developed  which 
may  enter  into  new  connective-tissue  formations.  The  na- 
ture of  the  subsequent  changes  will  depend  upon  the  inten- 
sity and  duration  of  the  inflammatory  process.  If  the  in- 
flammatory process  subsides  before  there  is  much  serous 
exudation,  and  the  two  surfaces  of  the  pleura  come  in  con- 
tact, adhesion  takes  place  ;  this  union  is  effected  in  the  fol- 
lowing manner : — the  new  cells  embedded  in  the  fibrous 
layer  become  elongated  and  spindle-shaped,  and  form  con- 
nective-tissue cells  ;  the  fibrin  fibrillates  and  a  net-work  of 
capillaries  permeate  the  young  false  membrane  ;  these  newly- 
formed  vessels  are  characterized  by  their  wide  calibre  and 
by  the  thinness  of  their  walls.  It  is  also  probable  that  in 
some  cases  union  may  take  place  without  the  intervention  of 
any  fibrinous  layer,  by  the  formation  and  growing  together 
of  papillary  outgrowths  from  the  subepithelial  tissue. 

The  serous,  fibrinous,  and  cellular  exudations  may  all 
undergo  absorption,  or  the  serous  exudation  may  be  ab- 
sorbed and  the  plastic  exudation  may  agglutinate  the  two 
pleural  surfaces  ;  whether  there  is  really  any  connective  tis- 
sue in  this  agglutination  is  a  question.  Not  unfrequently 
the  plastic  exudation  appears  to  agglutinate  the  pleural 


172  ETIOLOGY. 

surfaces  more  or  less  firmly,  and  to  form  something  analo- 
gous to,  if  not  identical  with,  recent  connective-tissue  ad- 
hesions. Generally,  however,  all  the  exudation  upon  the 
surface  of  the  pleura  and  the  exudation  which  is  found  at 
the  bottom  of  the  pleural  cavity  undergo  absorption. 
\Y  henever  the  pleural  surfaces  become  bound  together  by 
firm  adhesions,  these  adhesions  will  contain  wavy  bands  oi 
connective  tissue,  wThich  are  covered  by  a  single  layer  of 
pavement  epithelium,  within  which  run  long  slender  blood- 
vessels. These  adhesions  may  follow  the  general  law  that 
governs  all  new  connective  tissue,  and  be  permanent,  or 
they  may  contract  so  rapidly  as  to  shut  off  their  supply  of 
blood,  and  thus  interfere  with  their  nutrition ;  they  then 
undergo  fatty  metamorphosis,  and  are  absorbed,— the 
thickened  pleura  alone  remaining  to  tell  of  the  recent  in- 
flammation. 

ETIOLOGY.— The  etiology  of  primary  acute  pleurisy  is 
sometimes  very  obscure.  Exposure  to  cold  and  wet  has 
been  regarded  as  one  of  its  most  frequent  causes,  but  I 
doubt  if  it  ever  occurs  as  the  result  of  simple  exposure  to 
wet  and  cold ;  in  all  instances  where  it  has  followed  such  ex- 
posures, I  have  been  able  to  find  some  previously  existing 
predisposing  cause.  Occasionally,  you  will  meet  with  it  as 
the  direct  result  of  a  blow  or  some  other  injury  to  the  side. 

The  exciting  causes  of  acute  secondary  pleurisies  are  nu- 
merous. Among  the  most  common  are  pysemia,  the  exan- 
thematous  fevers,  alcoholismus,  acute  rheumatism  and  vis- 
ceral diseases,  as  pneumonia,  Bright' s  disease,  etc.  Some- 
times acute  pleurisy  occurs  as  the  result  of  an  extension  of 
inflammation  from  adjacent  tissues,  as  when  pleurisy  is 
secondary  to  pneumonia  and  pericarditis. 

Acute  pleurisy  may  occur  at  any  age.  Although  some 
authorities  have  claimed  that  it  has  never  occurred  in  young 
children,  it  is  of  quite  frequent  occurrence  in  children  of 
two  or  three  years  of  age,  and  my  experience  would  lead 
me  to  believe  that  pus  is  very  often  the  product  of  the  in- 
flammation in  the  pleurisies  of  children,  especially  when 
they  occur  as  sequelae  of  the  exanthematous  fevers. 

SYMPTOMS. — Acute  pleurisy  may  be  mild  or  severe ;  in 


ACUTE  PLETJEISY.  173 

either  case  it  is  ushered  in  by  well-marked  symptoms.  At 
its  onset  the  most  prominent  symptom  is  a  sharp,  stitch-like 
pain  in  some  portion  of  the  thoracic  wall ;  this  pain  in- 
creases in  severity  from  hour  to  hour ;  it  is  usually  most 
marked  under  the  nipple  of  the  affected  side.  Each  inspi- 
ration increases  its  severity,  consequently  the  respiration 
becomes  catching  in  character.  The  patient,  to  prevent 
motion  of  the  affected  side,  assumes  a  peculiar  position, 
leaning  forward  and  toward  the  affected  side.  Chills  are 
not  usually  present  in  the  early  stage  of  pleurisy.  At  first 
the  countenance  is  pale  and  anxious  ;  after  a  few  hours  it 
becomes  flushed.  The  pulse  is  accelerated,  beating  from 
ninety  to  one  hundred  and  twenty  per  minute  ;  it  is  firm, 
small,  and  tense  in  character  ;  in  this  respect  it  differs  from 
the  pulse  of  all  other  pulmonary  diseases.  The  respiration 
is  hurried  ;  each  inspiration  is  jerking  and  shallow  in  char- 
acter ;  as  soon  as  the  general  phenomena  of  pyrexia  are 
apparent,  in  most  cases  the  pain  diminishes,  in  a  few  it 
maintains  its  intensity. 

The  temperature  follows  no  regular  course,  and  bears  no 
fixed  relation  to  the  pulse  or  respiration  ;  in  ordinary  cases 
it  rarely  rises  above  100°  F.  I  have  occasionally  seen  the 
temperature,  in  acute  pleurisy,  reach  104°  F.  There  is  a 
constant,  teasing,  hacking  cough,  either  perfectly  dry  or 
accompanied  by  a  moderate  amount  of  thin  mucous  expec- 
toration. 

With  these  symptoms  there  is  nausea,  white  coating  of 
the  tongue,  thirst  and  anorexia ;  occasionally  vomiting  is 
present  in  the  early  stage. 

Very  severe  attacks  of  acute  pleurisy,  where  the  fibrinous 
exudation  is  abundant  and  takes  place  rapidly,  are  often 
ushered  in  by  very  active  symptoms,  very  like  the  com- 
mencement of  pneumonia ;  a  distinct  chill  is  followed  by 
high  fever,  or  several  chills  follow  each  other  in  succession  ; 
the  pain  in  the  affected  side  is  very  severe  ;  an  anxious  ex- 
pression of  countenance  will  be  developed,  which  is  very 
characteristic  ;  the  pulse  will  reach  120  per  minute,  and  is 
sometimes  feeble.  Under  these  circumstances,  at  the  onset 
of  the  attack,  there  may  be  some  difficulty  in  distinguishing 


174  PHYSICAL   SIGXS. 

such  cases  from  those  of  acute  pneumonia  ;  but  the  presence 
of  the  cough,  and  the  characteristic  expectoration  in  the 
pneumonia,  and  their  absence  in  pleurisy,  will  ordinarily  be 
sufficient  to  establish  a  diagnosis. 

As  the  disease  advances  in  these  severe  cases,  the  pain 
abates  or  altogether  ceases,  after  which  the  general  symp- 
toms are  the  same  as  those  of  the  milder  form,  except  that 
convalescence  is  slow,  as  it  takes  a  long  time  for  the  lung  to 
regain  its  normal  function  ;  sometimes  the  agglutination  of 
the  pleural  surfaces  is  so  extensive  that  the  lung  is  permanent- 
ly crippled,  and  retraction  of  the  affected  side  takes  place. 

Although  the  rational  symptoms  of  acute  pleurisy  are  not 
numerous,  they  are  sufficiently  characteristic  to  direct  your 
attention  to  the  seat  of  the  disease,  and  if  there  is  any  doubt 
remaining  with  regard  to  the  diagnosis,  the  physical  signs 
will  at  once  dispel  it. 

PHYSICAL  SIGXS. — In  order  that  the  physical  signs  of 
acute  pleurisy  may  be  more  readily  appreciated,  it  is  well  to 
divide  it  into  four  stages,  corresponding  to  its  anatomical 
changes. 

First,  a  dry  stage,  in  which  hypersemia  and  a  drying-up 
of  the  natural  lubricating  fluid  of  the  pleural  membrane  are 
the  principal  pathological  changes. 

Second,  a  plastic  stage,  in  which  there  is  more  or  less  abun- 
dant plastic  exudation  over  a  portion  or  the  entire  free  sur- 
face of  the  pleura, 

Tliird,  a  stage  of  effusion,  in  which  there  is  a  moderate 
amount  of  serum  with  lymph  poured  into  the  pleural  cavity. 

Fourth,  a  stage  of  absorption  and  adhesion,  in  which  the 
serum  and  lymph  disappear,  and  the  granulating  surfaces 
of  the  pleura  come  together,  and  adhesions  more  or  less  ex- 
tensive take  place. 

Ordinarily,  these  four  stages  can  readily  be  recognized  by 
their  attending  physical  signs.  We  will  first  study  the  phy- 
sical signs  of  the  dry  stage. 

Upon  inspection,  the  movements  of  the  chest- walls  on  the 
affected  side  will  be  found  more  or  less  restricted. 

Palpation,  percussion,  and  mensuration  furnish  nega- 
tive results. 


ACUTE  PLEURISY.  175 

On  auscultation,  the  respiratory  murmur  will  be  feeble 
over  the  affected  side,  but  rarely  entirely  absent.  The  respi- 
ration will  be  jerking  in  character,  on  both  inspiration  and 
expiration,  but  most  marked  on  inspiration.  Within  twelve 
hours  from  the  commencement  of  the  pleuritic  inflammation, 
to  the  feeble  and  jerking  respiration,  there  will  be  added  a 
grazing  friction-sound.  This  sound  will  be  most  intense  at 
the  end  of  inspiration  ;  it  lasts  only  a  few  hours,  and  disap- 
pears, perhaps  not  to  return  during  the  progress  of  the  case. 

In  the  second  stage,  or  stage  of  plastic  exudation,  you 
will  notice,  on  inspection,  that  there  is  still  greater  loss  of 
expansive  motion  on  the  affected  side.  You  will  also  notice 
that  now,  if  not  before  this,  the  patient  assumes  a  peculiar 
position ;  this  he  does  at  the  very  commencement  of  the 
plastic-  exudation  ;  his  object  is  to  prevent  motion  on  the 
affected  side,  consequently  he  will  bend  the  body  toward 
the  affected  side,  and  press  his  hands  against  the  thoracic 
wall  upon  that  side. 

In  acute  pleurisy  the  pain  usually  continues  during  the 
occurrence  of  the  plastic  exudation ;  it  may  continue 
throughout  the  entire  course  of  the  disease. 

On  palpation,  slight  loss  of  vocal  fremitus  will  be  ob- 
tained upon  the  affected  side,  over  the  seat  of  the  pleurisy. 

Percussion  will  reveal  slight  dulness  over  the  seat  of  the 
plastic  exudation.  The  amount  of  dulness  will  correspond 
to  the  amount  of  plastic  exudation,  so  that  the  amount  of 
plastic  material  may  be  determined  by  the  degree  of  dulness 
which  is  present. 

Upon  auscultation,  the  respiratory  murmur  will  be  found 
feeble,  or  entirely  absent.  A  crepitant  friction-sound  will 
be  heard  both  with  inspiration  and  expiration,  but  most 
marked  with  inspiration.  This  sound  resembles  very  closely 
the  subcrepitant  rale,  and  is  frequently  mistaken  for  it.  It 
is  heard  over  that  portion  of  the  chest-wall  which  corre- 
sponds to  the  seat  of  the  plastic  exudation,  and  always  has 
a  sticky  character. 

In  the  third  stage,  or  stage  of  effusion,  inspection  will  re- 
veal a  greater  loss  of  expansive  movement  on  the  affected 
side.  Palpation  will  determine  that  the  vocal  fremitus  is 


176  PHYSICAL   SIGXS. 

more  markedly  diminished ;  over  the  surface  of  the  fluid  it 
will  be  entirely  absent. 

Upon  percussion,  complete  flatness  will  be  obtained  as 
far  as  the  fluid  rises,  there  will  be  dulness  above  the  fluid, 
on  account  of  the  presence  of  plastic  material ;  the  fluid 
always  occupies  the  most  dependent  portion  of  the  pleura! 
sac.  It  is  difficult  to  recognize  the  presence  of  a  small 
quantity  of  fluid  in  the  pleural  cavity,  for  the  reason  that  a 
change  in  the  level  of  the  fluid  is  not  well  marked  in  con- 
nection with  a  change  in  the  position  of  the  body,  on  account 
of  the  plastic  material  which  usually  exists  just  above  the 
fluid. 

On  auscultation,  you  will  have  entire  absence  of  the 
respiratory  sounds  below  the  level  of  the  fluid ;  above  the 
level  of  the  fluid  you  will  have  a  feeble  respiratory  mur- 
mur, bronchial  in  character,  and  a  crepitating  friction-sound, 
the  same  as  in  the  stage  of  plastic  exudation.  In  very  many 
cases  these  sounds  continue  not  only  while  the  fluid  is  pres- 
ent, but  after  it  has  been  absorbed. 

Below  the  level  of  the  fluid,  the  vocal  sounds  are  feeble, 
or  entirely  abolished.  In  the  fourth  stage,  or  stage  of  ab- 
sorption and  adhesion,  on  percussion  there  is  a  gradual  re- 
turn of  the  pulmonary  resonance,  and  of  the  normal  vocal 
and  respiratory  sounds ;  as  the  two  roughened  surfaces 
of  the  pleura  come  together,  adhesions,  more  or  less  com- 
plete, are  formed. 

Inspection  will  still  show  diminished  respiratory  move- 
ments on  the  affected  side,  and  on  palpation  there  will 
still  be  diminished  vocal  fremitus.  The  percussion  sound 
will  become  less  and  less  dull,  as  the  fluid  and  plastic 
material  disappear.  On  auscultation  the  friction-sounds, 
which  may  have  been  absent  during  the  presence  of  the 
fluid  in  the  lower  portion  of  the  pleural  cavity,  will  again 
be  heard,  and  the  respiratory  sounds  will  become  more  and 
more  distinct.  In  some  instances  the  friction- sounds  re- 
main audible  for  some  time  after  the  disappearance  of  all 
other  signs  of  pleurisy. 

Retraction  of  the  affected  side  does  not  follow  acute  pleu- 
risy, except  in  rare  instances,  when  the  inflammation  has 


ACUTE  PLEURISY.  177 

been  very  severe,  and  a  large  amount  of  plastic  exudation 
has  been  effused  into  the  pleural  sac. 

DIFFERENTIAL  DIAGNOSIS. — In  the  majority  of  instances, 
the  diagnosis  of  acute  pleurisy  is  easily  made  ;  pneumonia 
is  the  only  disease  with  which  it  is  liable  to  be  confounded. 
In  both  affections  there  is  fever,  dyspnoea,  and  cough,  but 
in  pleurisy  the  temperature  rarely  rises  above  100°  F.,  while 
in  pneumonia  it  usually  reaches  103°  F.  within  the  first  twen- 
ty-four hours.  The  cough  of  pleurisy  is  short  and  hacking, 
and  is  attended  with  little  or  no  expectoration,  whereas,  in 
nearly  every  case  of  pneumonia,  expectoration  is  present, 
and  the  substance  expectorated  is  characteristic  of  pneu- 
monia. The  countenance  of  pleurisy,  at  first,  is  pale  and 
anxious,  while  in  pneumonia  it  is  flushed,  and  the  cheeks 
are  of  a  deep  purple  hue  ;  in  a  large  proportion  of  cases  of 
pneumonia,  the  expression  of  countenance,  twenty-four 
hours  after  the  commencement  of  the  disease,  will  enable 
you  to  make  a  correct  diagnosis. 

There  is  also  a  very  marked  difference  in  the  physical 
signs  of  the  two  diseases.  In  pleurisy,  the  vocal  fremitus 
over  the  affected  pleura  is  diminished  or  entirely  absent ;  in 
pneumonia,  it  is  more  or  less  increased.  In  pleurisy,  there 
is  feeble  or  absent  respiration ;  in  pneumonia,  it  is  rude  or 
bronchial.  In  pleurisy,  a  grazing,  rubbing,  or  crepitating 
friction-sound  is  heard  with  both  respiratory  acts ;  in  pneu- 
monia, the  crepitant  rale  is  heard  at  the  end  of  inspiration. 
Sometimes,  there  is  difficulty  in  distinguishing  a  crepitant 
friction-sound  from  a  subcrepitant  rale,  but  as  the  subcrepi- 
tant  rale  is  not  present  until  the  last  stage  of  pneumonia, 
the  differential  diagnosis  will  have  been  made  before  that 
period  arrives. 

Occasionally,  there  is  some  difficulty  in  making  a  differ- 
ential diagnosis  between  intercostal  neuralgia  or  pleuro- 
dynia  and  acute  pleurisy.  An  attack  of  intercostal  neu- 
ralgia or  pleurodynia  may  be  attended  by  nearly  all  the 
symptoms  of  acute  pleurisy  ;  it  may  come  on  after  exposure, 
be  attended  by  violent  pain  in  the  side,  jerking  respiration, 
bending  of  the  body  towards  the  affected  side,  anxiety  of 
countenance,  accompanied  by  an  amount  of  fever  not  incon- 
12 


178  TREATMENT. 

sistent  with  pleurisy.  On  physical  examination,  the  respi- 
ration may  be  as  feeble  as  in  the  first  stages  of  pleurisy  ;  the 
presence  or  absence  of  the  pleuritic  friction  alone  settles 
the  question.  You  will  often  be  unable  to  make  a  diag- 
nosis at  your  first  visit. 

PROGNOSIS. — In  acute  pleurisy,  the  prognosis,  with  refer- 
ence to  recovery,  is  good.  If  the  amount  of  plastic  exuda- 
tion is  not  abundant,  the  patient  may  be  positively  assured 
that  complete  recovery  will  take  place  within  a  few  weeks. 

If,  however,  the  pleurisy  is  complicated  by  any  grave 
form  of  disease,  such  as  septicaemia,  pneumonia,  or  pericar- 
ditis, the  complication  renders  the  prognosis  unfavorable. 
The  reason  for  an  unfavorable  prognosis  under  such  cir- 
cumstances consists  in  the  liability  to  the  development  of 
acute  empyemia. 

If  the  plastic  exudation  is  abundant,  and  is  not  rapidly 
absorbed,  it  may  undergo  cheesy  metamorphosis,  and 
become  the  exciting  cause  of  a  tuberculosis. 

TREATMENT. — The  only  remedial  agent  which  has  seemed 
to  me  to  have  a  controlling  power  over  acute  pleurisy  is 
opium.  The  best  method  of  administering  it  is  by  means 
of  a  hypodermic  injection  of  morphine  given  at  or  near  the 
seat  of  pain.  It  has  been  claimed  that  free  blood-letting  at 
the  commencement  of  an  acute  pleurisy  will  cut  short  its 
progress,  but  the  facts  deduced  from  recorded  cases  are 
strongly  against  this  statement.  A  free,  general  bleeding 
will  undoubtedly  relieve  the  pleuritic  pain  with  great 
promptitude,  but  no  more  so  than  a  hypodermic  injection  of 
morphine  ;  and  the  use  of  the  morphine  does  not  increase  the 
liability  to  large  serous  effusion,  as  does  a  general  bleeding. 

Clinical  experience  shows  that  this  disease  always  tends 
to  recovery  unless  an  abundant  serous  effusion  occurs,  and 
such  an  effusion  is  much  more  likely  to  occur  in  those  on 
whom  a  general  bleeding  has  been  practised. 

In  mild  as  well  as  severe  cases  of  pleurisy,  all  the  treat- 
ment which  will  be  required  for  the  successful  management 
of  the  disease  will  be  to  place  the  patient  in  bed  (and  this 
is  all-important  for  its  successful  management),  in  a  room 
with  a  temperature  of  about  65°  F.  The  patient  should  be 


ACUTE   PLEURISY.  179 

allowed  to  assume  tlie  posture  which  he  finds  the  most 
comfortable.  He  should  be  forbidden  all  unnecessary 
movements  and  talking,  and  a  nutritious  diet  without 
stimulants  should  be  given  him.  Apply  an  anodyne  poul- 
tice to  the  affected  side,  and  administer  hypodermic  in- 
jections of  morphine  in  quantities  sufficient  to  relieve 
all  pain.  Ordinarily,  at  the  expiration  of  four  or  five 
days  the  patient  will  be  able  to  sit  up,  and  within  two 
or  three  weeks  will  be  able  to  resume  his  ordinary  business. 
If  the  plastic  or  serous  exudation  is  abundant,  it  may 
require  two  or  three  weeks  for  its  absorption,  during  which 
time  it  is  better  that  the  patient  should  remain  in  bed  ;  at 
least,  he  must  keep  his  room  and  avoid  all  physical  exer- 
tion. In  these  cases,  the  lung  will  always  be  more  or  less 
crippled  ;  it  will  not  expand  to  its  normal  extent,  and  there 
will  be  slight  retraction  of  the  affected  side.  It  is  well  to 
tell  such  patients  of  the  expected  retraction,  and  of  the  con- 
sequent dyspnoea  from  which  they  will  probably  suffer  for 
five  or  six  months,  upon  taking  active  exercise. 

If  the  patient  is  at  all  anaemic,  the  syrup  of  the  iodide  of 
iron  should  be  given  in  teaspoonful  doses,  three  or  four 
times  each  day, — never  resort  to  stimulants  until  the 
second  or  third  week  of  the  disease.  In  the  treatment  of 
this  form  of  pleurisy,  all  the  so-called  "antiphlogistic 
remedies"  and  counter-irritants  are  to  be  avoided. 


LECTURE  XV. 


PLEURISY. 


Subacute  Pleurisy. 

AT  the  close  of  my  last  lecture  I  completed  the  history 
of  acute  pleurisy  ;  I  will  this  morning  pass  to  the  considera- 
tion of  a  much  more  common  form  of  pleurisy,  which  may 
be  designated  as  subacute.  You  will  meet  with  compara- 
tively few  cases  that,  strictly  speaking,  can  be  called  acute, 
while  the  subacute  variety  is  of  not  unfrequent  occurrence, 
and  often  for  weeks  passes  unrecognized.  In  city  practice 
we  meet  with  very  few  cases  of  acute  pleurisy. 

MORBID  ANATOMY. — The  anatomical  changes  which  take 
place  in  this  variety  of  pleurisy  are  similar  to  those  already 
described  as  taking  place  in  acute  pleurisy,  except  that  the 
new  tissue-formations  are  more  extensive,  the  pleura!  mem- 
brane more  uniformly  thickened,  and  there  is  a  more  abun- 
dant serous  effusion  containing  flocculi  of  lymph.  The 
plenral  cavity  may  be  partly  or  completely  filled  with 
serous  fluid,  in  which  are  flocculi  of  lymph,  and  a  few 
lymphoid  cells.  The  surface  of  the  pleura  is  more  or  less 
extensively  covered  with  a  membranous  exudation  composed 
of  fibrin  and  cells ;  sometimes  the  serous  effusion  contains 
blood-globules  from  the  rupture  of  the  thin-walled  vessels 
of  the  young  connective  tissue.  It  is  the  large  amount  of 
serous  effusion  containing  more  or  less  cellular  elements 
that  distinguishes  subacute  from  acute  pleurisy.  This 
marks  a  difference  in  the  grade  of  the  inflammatory  action 


SUBACTJTE  PLEUKISY.  181 

rather  than  a  difference  in  the  inflammatory  process.  Ordi- 
narily, the  cellular  element  is  not  very  abundant :  when 
cells  are  present  in  considerable  numbers,  they  characterize 
a  sero-puralent  effusion ;  the  serum  does  not  degenerate 
into  pus,  but  an  abundant  cell-formation  occurs  as  a  pro- 
duct of  the  pleuritic  inflammation.  If  the  pleural  cavity  is 
not  filled  with  fluid,  the  effusion  usually  occupies  the  most 
depending  portion  of  the  cavity  ;  it  may,  however,  be  con- 
fined to  other  portions  of  the  pleural  cavity  by  membranous 
adhesions.  If  it  occupy  the  lower  portion,  the  adjacent 
lung-tissue  will  be  compressed  and  pushed  upward. 

When  the  pleural  cavity  is  filled  with  fluid,  the  inter- 
costal spaces  will  be  more  or  less  distended, — the  diaphragm 
will  be  pushed  downward,  and  the  abdominal  viscera  upon 
either  side  may  be  displaced, — the  heart  will  be  displaced 
either  to  the  right  or  left,  according  as  the  fluid  occupies 
the  right  or  left  pleural  cavity.  The  lung  on  the  affected 
side  will  be  pushed  upward  and  inward  against  the  medias- 
tinum and  spinal  column.  It  may  be  compressed  to  one- 
eighth  of  its  natural  size  and  assume  a  pale-red  or  greenish 
color,  have  a  tough,  leathery  feel,  and  be  entirely  void  of 
air.  With  the  compression  of  the  lung  there  may  be  com- 
pression of  the  bronchial  tubes.  Occasionally,  some  of  the 
large  bronchial  tubes  remain  pervious  to  air,  and  then 
bronchial  respiration  will  be  heard  over  the  compressed 
lung. 

If  recovery  takes  place,  the  serum  readily  disappears  by 
absorption,  the  fibrin  undergoes  fatty  metamorphosis,  lique- 
fies, and  slowly  disappears.  As  the  fluid  disappears,  the 
thickened  pleural  surfaces  come  in  contact,  and  adhesions 
more  or  less  extensive  form  between  their  two  surfaces. 

On  account  of  the  thickening  of  pulmonary  pleura,  the 
lung-tissue,  although  it  receives  air,  does  not  expand  to  its 
normal  dimension,  and  retraction  of  the  chest-walls  follows. 
The  longer  the  fluid  remains  within  the  pleural  cavity,  the 
more  extensive  will  the  new  tissue-changes  in  the  pleura 
become,  and  the  more  marked  will  be  the  retraction  which 
will  follow. 

As  the  fluid  in  the  pleural  cavities  disappears,  the  organs 


J82  SYMPTOMS. 

which  have  been  displaced  return  to  their  normal  position. 
If  the  retraction  of  the  chest-walls  is  considerable,  the  liver 
may  rise  higher  than  normal,  and  the  heart  may  be  crowded 
out  of  its  normal  position  by  the  retraction.  In  some  cases, 
yellow,  cheesy,  or  calcareous  masses,  consisting  of  rem-, 
nants  of  unabsorbed  fibrin  and  cells  will  be  found  in  the 
pleural  cavity  embedded  in  a  mass  of  connective  tissue. 

ETIOLOGY. — Subacute  pleurisy  often  depends  upon  the 
causes  already  named  as  productive  of  acute  pleurisy, 
although  in  a  large  proportion  of  cases  it  is  secondary  to 
some  form  of  organic  disease,  as  chronic  Bright' s  disease  of 
the  kidney,  pulmonary  phthisis,  etc. 

Occasionally,  it  seems  to  occur  spontaneously,  or  at  least 
from  causes  not  well  understood. 

The  pathological  relations  of  those  cases  in  which  sub- 
acute  pleurisy  precedes  the  development  of  phthisis  are 
exceedingly  interesting  and  important. 

It  is  a  clinical  fact  familiar  to  every  careful  observer  that 
subacute  pleurisy  is  not  unfrequently  the  first  step  in  the 
development  of  phthisis. 

The  development  of  so-called  tubercles  in  the  pleura  is 
more  frequently  associated  with  the  development  of  acute 
than  of  subacute  pleurisy. 

The  weak  and  enfeebled  rather  than  the  strong  and 
robust  are  subject  to  attacks  of  subacute  pleurisy. 

SYMPTOMS. — The  symptoms  attending  this  form  of  pleu- 
risy are  usually  mild  in  character.  It  is  seldom  ushered  in 
by  a  distinct  chill ;  generally  it  comes  on  after  exposure  to 
wet,  cold,  and  fatigue,  in  those  who  are  in  a  debilitated  con- 
dition, or  already  suffering  from  some  chronic  form  of  dis- 
ease. It  is  rarely  attended  by  any  noticeable  pain,  at  least 
none  of  that  severe  pain  which  attends  acute  pleurisy  ; 
sometimes  pain  will  be  entirely  wanting.  On  close  ques- 
tioning, the  patient  will  state  that  some  time  before  he  had 
an  uneasy  sensation  in  the  affected  side,  attended  by  an 
occasional  sharp  pain  of  a  few  moments'  duration. 

This  form  of  pleurisy  is  often  so  insidious  in  its  approach 
that  the  patient  will  be  unable  to  tell  when  he  commenced 
to  be  sick  ;  gradually,  through  a  period  of  five  or  six  weeks, 


SUBACUTE   PLEURISY.  183 

he  has  noticed  that  he  was  not  feeling  quite  strong  and 
well,  not  that  he  has  been  really  ill ;  he  has  not  been  con- 
fined to  his  bed  at  any  time,  and  perhaps  if  his  accustomed 
avocation  has  required  but  little  physical  exertion,  he  has 
attended  to  his  daily  business.  He  has  noticed  that  he  was 
growing  pale,  and  has  lost  some  flesh  ;  has  had  slight  dysp- 
noea on  exertion  ;  has  noticed  a  slight  febrile  excitement  at 
night,  his  hands  becoming  dry,  and  has  complained  of 
thirst ;  has  coughed  some,  and  expectorated  a  small  quantity 
of  mucus  or  muco-purulent  material. 

When  he  consults  you,  probably  the  only  rational  symp- 
toms of  disease  which  he  will  present  will  be  a  frequent, 
small  pulse,  slight  heat  and  dryness  of  the  skin,  the  ordinary 
temperature  not  rising  above  101°  F. ;  his  countenance  will 
be  pale  and  anxious,  his  breathing  short  and  catching  in 
character.  When  he  attempts  to  speak,  especially  after 
moderate  exercise,  his  sentences  are  uttered  in  a  broken  and 
interrupted  manner.  He  will  be  unable  to  lie  comfortably, 
except  on  his  back  or  on  the  affected  side,  with  his  head 
elevated.  His  pulse,  usually  small  and  feeble,  will  be  found 
varying  from  110  to  120  beats  in  a  minute,  feeble,  and  he 
will  complain  of  no  pain.  In  a  word,  from  the  rational 
signs  you  will  be  unable  to  make  a  correct  diagnosis. 

Occasionally  you  will  meet  with  cases  of  subacute  pleu- 
risy which  at  the  onset  are  attended  by  active  symptoms 
similar  to  those  of  acute  pleurisy,  but,  after  a  few  days,  the 
febrile  symptoms  abate  but  do  not  entirely  subside,  and  the 
serous  effusion,  which  is  much  greater  than  ordinarily 
attends  acute  pleurisy,  for  a  time  continues  to  increase,  then 
seems  to  remain  stationary  for  a  number  of  days,  or  even 
weeks ;  then  suddenly  there  is  a  renewal  of  the  fever,  the 
dyspncea  is  much  increased,  the  cough  becomes  more  con- 
stant and  harassing,  the  patient  is  unable  to  lie  down,  and 
the  fluid  rapidly  increases  ;  in  twenty -four  hours  the  pleural 
cavity,  which  has  been  only  half  full  of  fluid,  becomes  dis- 
tended, and  the  dyspncea  is  so  great  and  the  danger  from 
collateral  hypersemia  and  cedema  of  the  other  lung  so  immi- 
nent, that  immediate  relief  is  demanded  b}^  paracentesis. 
If,  therefore,  the  objective  symptoms  of  this  form  of  pleu- 


184  PHYSICAL   SIGXS. 

risy  are  not  well-defined,  and  if  it  is  always  difficult  and 
often  impossible  to  make  a  diagnosis  from  them  alone,  the 
physical  signs  become  very  important.  There  is  perhaps  no 
disease,  except  that  of  pulmonary  emphysema,  in  which  the ' 
physical  signs  are  more  distinctive  than  in  subacute  pleu- 
risy. I  shall  therefore  give  the  physical  signs  in  detail. 

PHYSICAL  SIGNS. — When  the  pleural  cavity  is  only  par- 
tially filled  with  fluid,  the  amount  and  its  situation  will  be 
determined  by  the  same  physical  signs  which  determine  its 
presence  in  the  effusive  stage  of  acute  pleurisy  ;  these  have 
already  been  sufficiently  considered. 

When,  however,  the  pleural  cavity  is  nearly  or  complete- 
ly filled  with  fluid,  and  the  lung  compressed  against  the 
spinal  column,  the  capacity  of  the  pleural  cavity  is  neces- 
sarily increased  in  every  direction,  and  important  modi- 
fications in  the  physical  signs  take  place.  There  is  a 
marked  difference  in  the  physical  signs  in  this  condition 
and  those  present  in  the  effusive  stage  of  acute  pleurisy.  I 
will  invite  your  attention  to  these  differences. 

By  inspection,  you  will  notice  that  there  is  an  enlarge- 
ment of  the  affected  side,  and  a  bulging  of  the  intercostal 
spaces.  The  respiratory  movements  upon  the  affected  side 
are  changed  from  an  upward  and  outward  movement  to  a 
direct  up  and  down  motion  ;  while  on  the  unaffected  side, 
the  expansive  respiratory  movements  are  increased. 

If  the  effusion  is  within  the  left  pleural  cavity,  the  heart 
will  be  displaced  to  the  right,  and  the  apex -beat  may  be 
noticed  under  the  right  nipple.  If  it  occupies  the  right 
pleural  cavity,  the  apex-beat  will  be  carried  to  the  left, 
beyond  its  normal  position.  You  will  also  notice  that 
there  is  a  fulness  below  the  free  border  of  the  ribs,  with 
more  or  less  displacement  of  the  abdominal  viscera  down- 
ward. 

By  mensuration,  the  measurement  of  the  affected  side  at 
the  end  of  expiration  will  be  one  or  two  inches  greater  than 
that  of  the  healthy  side  ;  but,  at  the  end  of  inspiration,  there 
will  be  manifested  only  a  trifling  difference  between  the  two, 
sides.  The  expansive  movements  on  the  healthy  side  will 
also  be  found  to  be  two  or  three  inches  greater  in  inspi- 


SUBACUTE  PLEUKISY.  185 

ration  than  expiration  ;  while  upon  the  affected  side,  inspi 
ration  may  not  expand  the  chest-wall  more  than  half  an 
inch. 

Upon  palpation,  in  the  majority  of  cases,  there  is  com- 
plete absence  of  vocal  fremitus.  This  is  a  very  marked 
and  one  of  the  most  important  physical  signs  of  the  pres- 
ence of  fluid  in  the  pleural  cavity.  Upon  percussion  there 
will  be  flatness  over  the  whole  of  the  affected  side.  If  the 
pleural  cavity  is  filled  with  fluid,  the  flatness  will  extend 
beyond  the  normal  limits  of  the  lung  ;  if  the  cavity  is  not 
completely  filled,  the  flatness  will  extend  from  the  bottom 
of  the  cavity  to  a  level  of  the  fluid,  and  a  change  in  the 
position  of  the  patient  will  change  the  line  of  flatness. 
Upon  auscultation  there  is  usually  entire  absence  of  all 
respiratory  and  vocal  sounds  over  that  portion  of  the 
affected  side  which  is  occupied  by  the  fluid.  At  the  upper 
and  posterior  portion  of  the  pleural  cavity,  over  the  com- 
pressed lung-tissue,  you  will  not  unfrequently  have  bron- 
chial respiration  and  bronchophony  ;  this  bronchial  respi- 
ration is  sometimes  diffused  and  heard  over  the  whole  of  the 
posterior  portion  of  the  affected  side.  I  have  already  told 
you  that  bronchial  respiration  is  a  physical  sign  of  pulmo- 
nary consolidation  ;  but  now  you  are  asked  to  remember 
that  bronchial  respiration  is  sometimes  a  physical  sign  of 
compressed  lung,  when  the  pleural  cavity  is  filled  with  fluid. 

The  respiratory  sound  over  the  healthy  side  continues 
vesicular  in  character  ;  but  it  is  exaggerated. 

As  the  fluid  in  the  pleural  cavity  subsides,  inspection 
shows  that  the  enlargement  of  the  affected  side  is  disappear- 
ing, that  the  intercostal  spaces  are  regaining  their  normal 
condition,  and  that  on  the  affected  side  the  respiratory  move- 
ments are  to  some  extent  returning. 

Mensuration  also  shows  a  gradual  diminution  in  the 
measurement  of  the  affected  side,  until  it  becomes  even  less 
than  the  opposite  side,  and  there  is  a  gradual  return  of  the 
vocal  fremitus. 

On  percussion,  normal  pulmonary  resonance  will  be 
found  gradually  returning,  first  at  the  upper  portion  of  the 
pleural  cavity,  then  following  the  retiring  fluid.  Rarely 


186  PHYSICAL   SIGXS 

does  it  completely  return  until  some  time  after  the  fluid  has 
been  removed  ;  especially  is  this  the  case  in  regard  to  the 
inferior  portion  of  the  pleural  cavity,  owing  to  the  great 
accumulation  of  solid,  plastic  material,  or  to  the  condensa- 
tion of  lung-tissue. 

Upon  auscultation,  it  will  be  noticed  that,  as  the  fluid 
disappears,  the  vocal  and  respiratory  sounds  will  gradually 
return,  and  this  return  will  also  be  first  manifested  at  the 
upper  portion  of  the  pleural  cavity,  and  will  become  more 
and  more  distinct  as  the  fluid  disappears.  At  first,  these 
respiratory  sounds  are  weak  and  distant ;  gradually  they 
become  more  and  more  distinct,  although  they  often  remain 
harsh  in  character. 

When  the  two  surfaces  of  the  pleura,  thickened  by  new 
tissue-formations,  which  have  caused  them  to  assume  a 
roughened  condition,  again  come  together,  there  is  produced 
a  creaking,  rubbing  friction-sound,  as  the  two  surfaces  play 
upon  each  other.  These  rubbing  friction- sounds  may  be 
audible  for  months  after  all  fluid  has  been  removed  from  the 
pleural  cavity.  The  vocal  resonance  is  at  first  bronchopho- 
nic,  then  exaggerated,  and  finally,  normal  vocal  resonance 
is  returned.  The  heart,  with  the  adjacent  abdominal  viscera, 
usually  very  quickly  returns  to  its  normal  position. 

If,  as  sometimes  happens,  the  lower  portion  of  the  affected 
lung  remains  permanently  impervious  to  air,  as  is  very 
likely  to  be  the  case  when  the  fluid  has  remained  for  a  long 
time  in  the  pleural  cavity,  the  upper  portion  of  the  lung 
may  become  emphysematous.  This  is  a  fact  of  consider- 
able importance,  for,  under  such  circumstances,  the  emphy- 
sema is  compensatory,  and  the  percussion-sound  in  the 
infra-clavicular  space  will  have  a  tympanitic  quality,  and 
the  respiration  in  this  space  will  become  harsh  and  blowing 
from  prolonged  expiration,  forming  a  very  marked  contrast 
to  the  dulness  on  percussion  and  feeble  respiration  at  the 
lower  portion  of  the  affected  side. 

DIFFEKP:XTIAL  DIAGNOSIS. — In  uncomplicated  cases  of 
«ub acute  pleurisy,  usually  the  diagnosis  is  very  readily 
made. 

"Under  certain  circumstances,  it  may  be  confounded  with 


STTBACUTE   PLEUEISY.  187 

pneumonia  or  phthisical  consolidation  of  the  lung, — with 
enlargement  of  the  liver  or  spleen, — and  with  cancer  of 
the  lung  and  pleura.  It  is  also  possible  for  a  thoracic  aneu- 
rism to  become  developed  in  such  a  manner  as  to  be  mis- 
taken for  subacute  pleurisy. 

Pleurisy  with  effusion  may  be  distinguished  from  phthisi- 
cal and  pneumonic  consolidation  by  the  history  of  the  case, 
—by  the  absence  of  the  characteristic  expectoration  of 
pneumonia  and  phthisis, — and  by  the  lower  temperature 
which  accompanies  the  pleurisy. 

Upon  physical  examination,  it  may  be  distinguished  by 
the  presence  of  bulging  of  the  affected  side, — by  the  ab- 
sence of  vocal  fremitus, — by  the  flatness  of  the  percussion 
sound, — by  the  alteration  in  the  level  of  the  fluid  on  change 
of  the  position  of  the  patient, — and  by  the  absence  or  feeble- 
ness of  the  vocal  and  respiratory  sounds. 

The  bronchial  breathing  which  is  sometimes  heard  over 
a  pleural  cavity  filled  with  fluid,  differs  from  the  bronchial 
respiration  of  pneumonia  or  phthisical  consolidation ;  it  is 
more  diffuse  and  less  tubular  in  quality,  and  is  riot  attended 
by  moist  rales. 

In  phthisical  consolidation  the  progress  of  the  physical 
signs  is  usually  from  above  downward — in  pleuritic  effusion, 
they  advance  from  below  upward  ;  besides  phthisis  of  an 
entire  lung  rarely  exists  without  involving  the  opposite 
lung,  while  any  amount  of  pleuritic  effusion  may  exist  in 
one  pleuritic  cavity,  and  the  other  remain  unaffected. 

In  the  second  stage  of  pneumonia,  but  few  rales  may 
accompany  the  bronchial  respiration  and  the  dulness  on 
percussion  ;  in  the  bronchial  respiration  which  is  heard 
over  compressed  lung  from  pleuritic  effusion,  no  rales  are 
heard. 

If  the  physical  examination  is  not  carefully  made,  a  mis- 
lake  may  very  easily  occur,  even  with  the  knowledge  of 
these  differences.  You  must  recollect  that  vocal  fremitus 
is  a  most  important  differential  physical  sign  ;  in  pleurisy 
it  will  be  absent,  in  pneumonia  it  will  be  intensified. 

Serous  effusion  into  the  right  pleural  cavity  is  distin- 
guished from  enlargement  of  the  liv^er  upward,  by  the  fact 


188  DIFFERENTIAL  DIAGNOSIS. 

that  when  percussion  is  made,  the  line  of  flatness  in  liver  en- 
largements is  higher  in  front  than  behind.  The  liver  does 
not  enlarge  in  such  a  manner  as  to  fill  the  pleural  cavity 
posteriorly  and  anteriorly  to  the  same  level.  This  is  the 
most  reliable  physical  sign  in  making  a  differential  diag- 
nosis between  subacute  pleurisy  and  enlargement  of  the 
liver. 

It  is  almost  impossible  to  mistake  enlargement  of  the 
spleen  for  subacute  pleurisy  of  the  left  side,  for  when  the 
spleen  is  but  slightly  enlarged,  the  enlargement  is  downward 
as  well  as  upward,  and  as  soon  as  it  has  reached  any  con- 
siderable size,  it  will  appear  in  the  abdominal  cavity  ;  then 
continuous  dulness  on  percussion  \vill  be  obtained  from  the 
limit  of  the  enlargement  in  the  abdominal  cavity  upward 
into  the  axillary  region  as  far  as  the  axillary  enlargement 
may  extend.  Again,  the  free  margin  of  the  enlarged  spleen 
generally  can  be  recognized  by  palpation,  and  the  lower 
margin  of  the  splenic  tumor  can  be  felt,  and  the  percussion 
dulness  will  extend  from  one  cavity  to  another. 

Differential  diagnosis  of  subacute  pleurisy  and  cancer  of 
the  lung  is  sometimes  impossible,  when  the  rational  symp- 
toms and  the  physical  signs  are  the  only  means  employed. 
We  can  decide  all  such  doubtful  cases  with  a  degree  of  cer- 
tainty by  the  explorative  puncture.  With  the  needle  of  a 
hypodermic  syringe,  it  is  possible  to  puncture  the  thoracic 
cavity  without  the  least  apprehension  of  damage,  whether 
the  needle  shall  enter  a  pleuritic  effusion,  a  hepatized  lung, 
a  cancer  of  the  pleura,  or  an  aneurism, — and  by  withdraw- 
ing the  piston  of  the  syringe  after  the  needle  has  entered 
the  pleural  cavity,  we  may  determine  positively  whether  the 
cavity  contains  fluid,  and,  if  fluid  is  present,  what  is  the 
character  of  the  fluid. 

PROGNOSIS.' — The  prognosis  in  uncomplicated  subacute 
pleurisy,  not  associated  with  phthisis,  and  not  secondary 
to  any  other  form  of  acute  or  chronic  disease,  is  good. 

When,  however,  the  effusion  has  taken  place  rapidly,  or 
when  there  is  great  distention  of  the  pleural  cavity,  whether 
the  effusion  has  taken  place  rapidly  or  slowly,  it  must  be 
remembered  that  there  is  danger  that  sudden  dyspnoea  may 


STJBACUTE  PLEURISY.  189 

occur,  wliicli  results  from  over-distention  of  the  pleural  cavi- 
ty ;  under  such  circumstances  the  prognosis  is  very  unfav- 
orable, unless  you  are  thoroughly  aroused  to  the  danger 
and  employ  the  proper  means  for  its  relief.  The  relief  con- 
sists in  the  immediate  performance  of  paracentesis  thoracis. 

The  development  of  pulmonary  emphysema  occasionally 
follows  a  subacute  pleurisy,  and  must  be  remembered  in 
order  to  make  an  intelligent  prognosis. 

Phthisical  developments  not  unfrequently  follow  sub- 
acute  pleurisy,  and  such  liabilities  must  be  taken  into  ac- 
count in  making  a  prognosis. 

An  individual  with  a  hereditary  or  an  acquired  tendency 
to  phthisis  may  have  an  extensive  serous  effusion  in  one 
pleural  cavity,  which,  if  permitted  to  remain  any  length  of 
time,  will  not  only  cause  permanent  crippling  of  the  lung, 
but,  as  the  result  of  degenerative  processes  set  up  in  the 
solid  inflammatory  products,  the  pleura  or  the  new  tissue 
formations  may  become  the  seat  of  tubercular  develop- 
ments. 

In  subacute  pleurisy,  a  sero-albuminous  fluid  effusion 
may  become  a  purulent,  or  rather  the  inflammatory  process 
which  furnishes  a  serous  effusion  becomes  changed  to  one 
that  gives  pus  as  its  product.  This  occurrence  is  of  serious 
import. 


LECTURE    XVI. 


PLEURISY. 


Subacute  Pleurisy  (continued). — Chronic  Pleurisy. 

I  SHALL  this  morning  continue  the  history  of  subacute 
pleurisy  by  inviting  your  attention  to  its  treatment. 

It  is  quite  evident  that  the  main  thing  to  be  accomplished 
in  the  treatment  of  this  disease  is  the  removal  of  the  fluid 
effusion  as  rapidly  as  possible,  at  the  same  time  taking  care 
to  sustain  the  vital  powers  of  the  patient. 

The  principal  means  which  have  been  employed  for  the 
removal  of  the  fluid  are  hydragogue  cathartics,  diuretics, 
diaphoretics,  and  blisters  applied  in  succession  over  different 
portions  of  the  affected  side.  On  account  of  the  anaemic 
condition  of  this  class  of  patients,  general  and  local  bleed- 
ing, as  well  as  mercurialization,  are  rarely  if  ever  employed. 
It  is  on  account  of  this  condition  that  I  very  much  question 
the  beneficial  effects  claimed  for  cathartics,  diuretics,  and 
blisters, — and  I  also  question  the  possibility  of  bringing 
about  the  condition  upon  which  the  absorption  of  the  pleu- 
ritic effusion  depends,  by  any  of  the  so-called  depurative 
remedial  agents.  The  principle  upon  which  the  depurative 
plan  of  treatment  is  based  is  as  follows  :  it  is  claimed  that 
hydragogue  cathartics  and  diuretics  have  a  tendency  to 
quickly  remove  large  quantities  of  fluid  from  the  system, 
and  consequently  the  fluid  portion  of  the  blood  is  greatly 
diminished, — so  that  whenever  fluid  exists  in  a  cavity,  the 
absorbents  and  blood-vessels  of  the  part  take  it  up  to  re- 
place the  loss,  and  the  absorption  of  fluid  from  a  pleural 


SUBACUTE  PLEURISY.  191 

cavity  is  thus  promoted.  There  perhaps  is  little  doubt 
but  that  hydragogue  cathartics  and  diuretics  will  hasten 
the  absorption  of  the  non-inflammatory  serous  effusion  in 
simple  hydrothorax  ;  but  it  is  by  no  means  certain  that 
they  have  the  same  power  in  promoting  the  absorption  of 
the  inflammatory  products  which  are  poured  out  into  the 
pleura!  cavity  in  subacute  pleurisy.  It  is  well  established 
that  by  the  action  of  these  depurative  agents  the  vital 
powers  are  greatly  enfeebled,  and  the  processes  of  digestion 
and  nutrition  are  more  or  less  interfered  with.  We  also 
know  that  when  the  nutritive  processes  are  going  on  most 
rapidly,  absorption  takes  place  most  rapidly ;  consequent- 
ly anything  that  interferes  with  these  processes  is  contra- 
indicated  when  we  wish  to  accomplish  the  absorption  of 
inflammatory  products. 

Again,  there  are  other  conditions  which  greatly  impede 
the  absorption  of  the  serous  effusion  in  pleurisy.  If  the 
pleural  cavity  is  distended  with  fluid,  its  absorption  is  im- 
peded by  the  obstruction  to  the  flow  of  blood  through  the 
vessels  of  the  compressed  lung,  as  well  as  by  the  capillary 
engorgement  beneath  the  pleura,  the  result  of  the  com- 
pression of  the  subpleural  veins,  and  if  there  is  bulging  of 
the  intercostal  spaces,  there  will  also  be  obstruction  to  the 
intercostal  venous  circulation.  Under  these  circumstances, 
it  is  evident  that  it  is  folly  to  expect  that  the  absorption  of 
the  fluid  will  be  promoted  by  the  use  of  diuretics  or  hydra- 
gogue cathartics.  The  mechanical  withdrawal  of  a  sufficient 
amount  of  liquid  to  relieve  the  tension  of  the  cavity,  and 
remove  pressure  from  lung  and  veins  beneath  the  pleura,  is 
an  absolute  necessity  before  the  process  of  absorption  can 
commence.  Again,  if  the  surface  of  the  pleura  is  covered 
by  a  thick  layer  of  fibrin,  this  layer  is  interposed  between 
the  subpleural  vessels  and  the  liquid  effusion,  and  must 
consequently  greatly  impede  the  absorption  of  the  liquid. 

In  describing  the  morbid  anatomy  of  this  form  of  pleurisy, 
I  stated  to  you  that  after  fluid  effusion  has  taken  place,  the 
false  membranous  layer  on  the  surface  of  the  pleura  becomes 
thicker  and  thicker  by  successive  deposits  of  fibrin  from  the 
liquid  effusion.  It  is  therefore  obvious  that  the  longer  the 


192  TREATMENT. 

liquid  effusion  remains  in  the  pleural  cavity,  the  greater  is 
the  probability  of  a  copious  deposit  of  fibrin  on  the  surface 
of  the  pleura,  and  the  thicker  this  fibrinous  deposit  becomes, 
the  less  is  the  probability  that  the  liquid  will  be  absorbed  ; 
for  this  reason  it  is  also  evident  that  cathartics  and  diuret- 
ics are  powerless. 

My  own  clinical  experience  has  sustained  these  views  in 
regard  to  the  failure  of  cathartics,  diuretics,  and  blisters 
to  remove  the  fluid  effusion  in  subacute  pleurisy.  During 
the  past  three  years  I  have  rarely  employed  any  of  these 
agents  in  the  treatment  of  pleurisy.  I  have  found  iron  to 
be  the  remedial  agent  which  has  the  greatest  power  in  pro- 
moting the  process  of  absorption.  The  statement  which 
has  been  made  by  very  competent  observers,  that  the  free 
internal  administration  of  the  syrup  of  the  iodide  of  iron 
assists  in  a  most  remarkable  manner  the  absorption  of  the 
inflammatory  products  from  the  pleural  cavity,  I  believe 
will  be  found  to  hold  true  in  a  large  proportion  of  cases. 
In  connection  with  the  internal  administration  of  iron,  the 
largest  amount  of  the  most  nutritious  food  should  be  fur- 
nished to  the  patient ;  a  bottle  of  wine  daily  is  also  very 
beneficial  to  this  class  of  patients.  The  principle  of  treat- 
ment is  to  raise  the  nutritive  processes  to  the  highest  pos- 
sible point,  and  all  the  remedial  and  hygienic  measures 
which  act  in  this  direction  must  be  employed. 

If,  then,  so  little  can  be  done  by  medication  to  excite  or 
even  hasten  the  absorption  of  pleuritic  effusion,  the  ques- 
tion arises,  Is  it  best  to  remove  it  by  mechanical  means  ? 
There  are  two  opinions  as  to  the  propriety  of  this  method 
of  procedure.  One  class  of  observers  claim  that  the  danger 
from  admitting  air  into  the  pleural  cavity  by  the  operation 
of  paracentesis  is  so  great,  that  it  should  rarely  if  ever  be 
resorted  to,  and  this  class  contend  that  by  allowing  air  to 
enter  the  pleural  cavity  while  fluid  is  being  withdrawn,  a 
serous  effusion  is  changed  into  a  purulent  one,  and  thus 
life  is  jeopardized.  On  the  other  hand,  the  advocates  of  the 
operation  maintain  that  if  the  fluid  is  permitted  to  remain 
in  the  pleural  cavity,  after  a  time  it  becomes  purulent,  and 
thus  many  lives  are  lost. 


SUBACUTE  PLEUKISY.  193 

The  statements  which  I  have  already  made  as  to  the  causes 
which  impede  or  render  impossible  the  absorption  of  the 
fluid  in  subacute  pleurisy,  seem  to  me  to  favor  early  tap- 
ping in  all  cases  where  there  is  copious  liquid  eif  usion. 

The  introduction  of  the  aspirator  has  inaugurated  a  new 
era  in  the  management  of  this  class  of  cases,  and  has  re- 
moved all  objection  to  the  early  withdrawal  of  these  fluid 
accumulations  by  mechanical  means.  When  a  perfect  in- 
strument is  used,  and  a  small  needle  introduced  into  the 
thoracic  cavity,  the  entrance  of  air  during  the  operation  is 
almost  an  impossibility.  There  are  some  who  believe  that 
the  entrance  of  air  into  the  pleural  cavity  is  an  unimportant 
accident,  but  this  I  believe  to  be  a  mistake. 

In  any  case  of  pleurisy,  when  the  fluid  accumulation  re- 
mains stationary  for  one  week,  or  is  increasing  after  the 
cavity  is  half  filled  with  fluid,  and  especially  when  the  cav- 
ity is  distended  with  fluid,  I  would  advise  to  aspirate  the 
chest.  Every  day  that  the  lung  remains  compressed,  and 
the  thicker  the  plastic  material  becomes  upon  the  pleural 
surfaces,  the  chances  of  its  absorption  are  diminished,  and 
the  greater  the  danger  of  permanent  crippling  of  the  lungs. 

The  following  rules  should  be  observed  in  the  perform- 
ance of  aspiration  of  the  chest.  Place  the  body  of  the  pa- 
tient in  an  erect  posture,  leaning  somewhat  forward,  with 
the  arm  of  the  aifected  side  thrown  partially  across  the 
chest, — this  position  of  the  arm  is  preferable  to  any  other, 
for  the  reason  that  the  integument  is  not  made  unnaturally 
tense  over  the  intercostal  spaces.  Select  a  needle  of  smai  t 
size  for  the  first  tapping,  and  introduce  it,  at  least  to  the 
depth  of  one  inch  into  the  fifth  or  sixth  intercostal  space  at 
the  junction  of  the  axillary  and  infra -scapular  regions. 
After  the  needle  has  been  introduced,  the  fluid  may  be  per- 
mitted to  flow  through  the  instrument  until  the  patient 
complains  of  a  sense  of  constriction  about  the  chest,  when 
you  must  immediately  stop  the  withdrawal  of  the  fluid. 
The  amount  of  fluid  that  can  be  removed  at  the  first  tapping 
will  depend  upon  the  length  of  time  the  fluid  has  occupied 
the  pleural  cavity.  If  it  has  accumulated  rapidly,  fre- 
quently the  cavity  may  be  emptied  without  giving  rise  to 
13 


194  MORBID  ANATOMY. 

any  unpleasant  symptoms  ;  if,  however,  it  has  been  slow  in 
its  accumulation  and  the  pleural  cavity  for  a  considerable 
time  has  contained  a  large  quantity  of  fluid,  only  a  small 
amount  can  be  withdrawn  without  producing  a  severe  at- 
tack of  dyspnoea.  When  this  is  the  case,  the  patient  may 
be  permitted  to  remain  quiet  for  one  or  two  days,  then  the 
operation  should  be  repeated,  so  often  as  it  can  be  without 
giving  rise  to  unpleasant  symptoms,  until  all  the  fluid  has 
been  removed.  The  sensation  of  constriction  about  the  chest 
always  indicates  that  no  more  fluid  should  be  withdrawn  at 
that  time. 

I  have  no  doubt  but  that  the  timely  performance  of  aspi- 
ration in  a  large  number  of  cases  of  subacute  pleurisy,  not 
only  has  tended  to  promote  rapid  recovery,  but  has  pre- 
vented those  changes  in  the  pleura  which  lead  to  a  tedious 
convalescence  and  incomplete  ultimate  recovery,  with  more 
or  less  contraction  of  the  affected  side,  the  lung  being  bound 
down,  and  its  expansion  prevented  by  the  excessive  pleu- 
ritic thickenings  and  adhesions. 

CHRONIC  PLEURISY  (Empyema). 

I  will  now  pass  to  the  consideration  of  another  form  of 
pleurisy,  which  I  have  designated  chronic  pleurisy,  or  em- 
pyema.  By  this  term  is  meant  an  inflammation  of  the 
pleural  membrane,  in  which  pus  is  the  product  of  the  in- 
flammatory action.  It  is  a  suppurative  inflammation,  which 
may  be  primary  or  secondary.  When  it  is  primary  it 
sometimes  commences  as  an  acute  affection ;  secondary 
suppurative  pleurisies  are  always  chronic. 

MORBID  AXATOMY. — In  primary  suppurative  pleurisies, 
as  in  all  active  inflammations  of  serous  membranes,  we  have 
poured  out  as  one  of  its  products  a  large  amount  of  plastic 
material.  This  plastic  material  undergoes  histological  trans- 
formations into  pus ;  such  transformations  are  especially 
liable  to  occur  in  septic  and  pysemic  pleurisies.  It  is  not 
altogether  an  unfrequent  occurrence  for  a  large  amount  of 
pus  to  be  rapidly  formed  in  the  pleural  cavity  in  connection 
with  cases  of  pyaemia.  The  following  is  the  rationale  of 
the  purulent  exudations  under  such  circumstances : 


CHRONIC   PLEURISY.  195 

With  the  sero-fibrinous  exudation  a  large  number  of 
white  corpuscles  migrate  from  the  dilated  blood-vessels, 
and  infiltrate  the  connective-tissue  of  the  pleura  as  well  as 
the  fibrinous  exudation  upon  its  surface,  from  which  they 
are  washed  by  the  serous  effusion  into  the  pleural  cavity, 
and  these  are  held  in  suspension  as  pus-corpuscles,  filling 
up  more  or  less  completely  the  cavity.  In  this  way  the 
pleuritic  effusion  becomes  purulent  on  its  way  from  the 
blood-vessels  to  the  free  surface  of  the  pleura.  Sometimes 
the  proportion  of  cells  present  in  the  exudation  will  be  very 
large,  and  very  rapidly  developed  ;  this  is  characteristic  of 
the  exudation  in  pleurisies  which  occur  in  connection  with 
pyaemia.  The  rapid  development  of  so  large  a  number  of 
cells  under  such  circumstances,  can  only  be  satisfactorily 
explained  on  the  ground  that  they  are  white  blood-globules. 

At  an  early  stage  of  the  process,  while  the  corpuscular 
exudation  is  moderate  in  amount,  the  exudation  is  clear, 
and  deposits  an  abundance  of  fibrinous  flakes ;  at  a  later 
stage,  it  consists  of  a  yellow,  or  greenish-yellow  pus,  giving 
rise  to  a  condition  which  may  be  termed  primary  empyema. 
On  the  other  hand,  a  sero-fibrinous  pleurisy  may  become 
purulent  when  a  fresh  source  of  irritation  is  established, 
which  gives  rise  to  an  active  cell-formation.  When  this 
transformation  takes  place,  the  first  noticeable  change  will 
be  a  new  inflammatory  action,  dependent  upon  a  new  irrita- 
tion. The  new  irritation  may  come  from  the  admission 
of  air  into  the  pleural  cavity,  or  from  some  change  in  the 
fluid  which  has  already  been  occupying  the  cavity,  or 
perhaps  from  some  suddenly  developed  septic  condition. 
Under  these  circumstances,  a  variety  of  cell-formative  pro- 
cesses are  established ;  some  are  produced  in  the  serous 
effusion,  some  in  the  plastic  exudation,  and  some  in  the 
pleura  itself.  The  clear  serum  becomes  turbid,  whole  shreds 
of  false  membrane  are  loosened  from  their  connection  with 
the  underlying  tissue,  and  undergo  liquefaction,  and  the 
whole,  or  a  large  portion  of  the  pleural  membrane,  becomes 
a  suppurating  surface,  and  we  have  the  pleural  surface 
changed  into  what  is  known  as  a  pyogenic  membrane,  and 
thus  a  large  amount  of  pus  may  be  formed  in  the  pleural 


196  MORBID   ANATOMY. 

cavity.  It  is  evident  that  if  the  irritant  be  a  mild  one,  there 
will  be  a  correspondingly  moderate  amount  of  cell-produc- 
tions ;  it  may  be  circumscribed,  and  not  general.  We  then 
have  a  sero-purulent  effusion  into  the  pleura!  cavity,  and  if 
the  chest  is  aspirated  during  this  stage  of  the  process,  the 
fluid  removed  will  be  found  to  contain  a  moderate  number 
of  cells,  no  more  than  is  often  present  in  what  is  ordinarily 
termed  a  serous  effusion. 

At  a  second  operation,  ten  days  or  two  weeks  later,  a 
large  number  of  cells  may  be  found,  and  on  this  account 
it  is  quite  common  to  condemn  the  operation,  because  there 
is  an  increase  in  the  number  of  cells  in  the  fluid  at  the 
second  tapping,  attributing  the  increase  to  the  first  opera- 
tion. This,  however,  is  not  a  legitimate  inference,  for  the 
increase  in  the  cell-development  is  the  natural  result  of  the 
morbid  processes  which  were  in  operation  at  the  first  tap- 
ping. The  fact  that  the  cell-production  is  rapidly  increasing, 
is  an  indication  that  the  fluid  should  be  removed  as  speedily 
as  possible  ;  at  the  same  time  an  earnest  endeavor  should 
be  made  to  find  out,  and  if  possible  remove,  the  cause  which 
may  be  giving  rise  to  the  increased  cell-productions.  The 
treatment  of  this  class  of  cases  will  be  decided  to  a  very 
great  extent  by  the  character  of  the  fluid  removed  from  the 
pleural  cavity.  Purulent  accumulations  in  the  pleural 
cavity  may  become  so  large  that  death  may  ensue  in  con- 
sequence of  the  depression  induced  by  their  presence. 
These  accumulations  may  also  escape  from  the  pleural 
cavity  by  spontaneous  openings, — the  chest- wall  may  be 
perforated  by  a  process  of  ulceration,  and  the  contents  of 
the  pleural  sac  be  discharged  externally  ;  or  the  lung  may 
be  perforated,  and  the  discharge  take  place  through  a  bron- 
chial tube  ;  or,  in  rare  instances,  the  diaphragm  may  be 
perforated,  and  the  pus  find  its  way  into  the  abdominal 
cavity,  which  usually  gives  rise  to  a  rapidly  fatal  peri- 
tonitis. 

Preceding  the  perforation  into  the  abdominal  cavity, 
sometimes  adhesions  take  place  between  the  intestines  and 
the  diaphragm,  and  in  this  way  the  pus  may  be  discharged 
into  the  intestinal  canal.  If  the  patient  survives  the  empty- 


CHEONIC   PLEUEISY.  197 

ing  of  the  pleural  cavity,  repair  is  accomplished  by  the 
rapid  and  abundant  formation  of  cicatricial  tissue ;  the 
pleural  cavity  is  contracted  in  every  direction  like  a  huge 
cicatrix,  the  chest-walls  of  the  affected  side  retract  to 
their  fullest  extent,  the  thoracic  and  abdominal  viscera  are 
dragged  out  of  their  normal  position  to  help  fill  up  the 
space  formerly  occupied  by  the  collapsed  and  indurated 
lung.  The  fibroid  sac  into  which  the  pleura  has  been  con- 
verted, goes  on  contracting  until  entire  obliteration  of  the 
pleural  cavity  is  accomplished,  and  then  the  purulent  dis- 
charge ceases. 

In  rare  instances,  purulent  accumulation,  or  rather  the 
fluid  portion  of  the  pus  in  the  pleural  cavity,  undergoes 
absorption.  In  those  cases  where  recovery  is  obtained 
without  any  opening  into  the  pleural  cavity,  usually  the 
solid  constituent  of  the  purulent  fluid  accumulates  in  the 
most  depending  portion  of  the  pleural  sac,  and  there  be- 
comes cheesy,  or  in  some  cases  becomes  calcareous.  The 
bony  or  calcareous  plates  in  the  pleural  cavity,  which  are 
occasionally  met  with  at  post-mortem  examinations,  most 
frequently  have  their  origin  in  connection  with  empyema. 
Sometimes  circumscribed  collections  of  pus  form  between  the 
pulmonary  and  costal  or  diaphragmatic  pleura,  entirely 
shut  in  by  adhesions  ;  such  collections  may  occur  in  any 
portion  of  the  pleural  cavity ;  they  are,  however,  most 
likely  to  be  met  with  at  its  most  depending  portion. 

ETIOLOGY. — In  every  case  of  chronic  pleurisy  or  empyema 
the  cause  cannot  be  ascertained.  Occasionally,  it  may  be 
of  traumatic  origin.  When  it  occurs  spontaneously,  it  is 
always  associated  with  some  vice  of  constitution,  such  as 
results  from  protracted,  exhausting  disease,  or  the  debility 
which  attends  chronic  alcoholismus  and  follows  enervating 
habits. 

It  has  not  been  clearly  shown  why  pleuritic  inflammation 
furnishes  pus  as  its  product  in  one  case,  and  only  serum 
and  flocculi  of  lymph  in  another  ;  in  both  cases  the  dis- 
ease being  equally  prolonged,  and  the  patients  in  an  equally 
enfeebled  condition. 

Clinical  observation  shows  that  a  suppurative  inflamma- 


198  SYMPTOMS. 

tion  of  the  pleura  may  sometimes  follow  and  depend  upon 
a  serous  and  fibrous  inflammation  ;  but,  in  such  cases,  it  is 
quite  evident  that  the  establishment  of  the  suppurative  pro- 
cess is  due  either  to  constitutional  changes  in  the  patient,  or 
to  some  new  local  excitement  of  the  inflammation.  Nearly 
all  of  the  pleurisies  that  are  developed  in  advanced  phthisis 
are  purulent  in  character. 

SYMPTOMS. — The  symptoms  of  empyema  are  very  ob- 
scure. The  presence  of  pus  in  the  pleural  cavity  is  not 
easily  recognized,  either  by  physical  signs  or  rational  symp- 
toms. Usually  it  is  not  difficult  to  determine  the  presence 
of  fluid  in  a  pleural  cavity,  but  you  are  often  unable  to  de- 
cide, except  by  the  exploring  trocar,  whether  that  fluid  is 
pus  or  serum. 

The  patient  rarely  suffers  from  local  pain, — there  is  simply 
a  sense  of  uneasiness  or  weight  in  the  affected  side.  There 
is  loss  of  flesh  and  strength,  and  the  patient  gradually 
grows  pale ;  the  countenance  wears  a  peculiar  pale,  anxious 
expression  ;  there  is  an  irregular  diurnal  fever  preceded  by 
a  chill,  and  followed  by  a  profuse  sweat.  Ordinarily,  the 
patient  has  a  cough  with  muco-purulent  expectoration,  not 
very  abundant, — his  voice  is  weak,  and  his  dyspnoea  is 
generally  slight,  for  the  process  has  been  of  such  slow  de- 
velopment, that  he  has  become  accustomed  to  the  crippled 
condition  of  the  lung,  and  the  healthy  lung  has  become  ac- 
customed to  its  additional  labor. 

As  the  disease  advances,  the  patient  assumes  more  and 
more  the  aspect  of  one  in  the  last  stages  of  pulmonary 
phthisis.  At  this  advanced  period,  it  will  be  impossible  to 
make  a  differential  diagnosis  between  the  two  diseases  by 
the  rational  symptoms  alone  ;  indeed,  the  two  conditions  are 
quite  often  associated. 

If  empyema  occurs  in  connection  with  or  follows  as  the 
result  of  septicaemia  or  pyaemia,  its  commencement  is 
equally  insidious.  In  these  conditions  patients  may  pass 
into  a  semi-comatose  state,  owing  to  the  serious  implica- 
tion of  the  nervous  system,  and  the  blunted  condition 
of  the  sensitive  nerves ;  so  that  not  unfrequently  pysemic 
patients  make  no  complaint  which  would  lead  you  to  the 


CHEOJSTIC   PLEURISY.  199 

pleura.  In  this  class  of  patients  you  will  sometimes  find 
the  pleura  two-thirds  full  of  pus,  without  a  single  objective 
symptom  which  would  lead  you  to  examine  the  pleural 
cavity. 

If  an  empyema  is  about  to  open  externally,  it  will  usu- 
ally make  itself  manifest  by  the  appearance  of  a  protrusion 
between  the  ribs,  which  gives  a  sense  of  fluctuation,  and 
after  a  time  grows  red  at  the  top  of  the  elevation,  and 
finally  a  valvular  opening  forms,  and  pus  is  discharged.  If 
the  opening  is  to  be  through  the  lung  into  a  bronchial  tube, 
the  discharge  of  pus  is  ordinarily  preceded  by  symptoms  of 
pneumonia. 

At  the  onset,  the  patient  will  probably  have  a  chill,  cough, 
and  more  or  less  profuse  expectoration  which  contains  some 
blood  ;  soon  after,  he  will  commence  expectorating  pus, 
perhaps  at  first  in  large  quantities  ;  this  will  be  followed  by 
marked  relief  ;  as  the  expectoration  goes  on,  retraction  of 
the  chest-walls  will  be  developed, — he  will  have  more  or  less 
profuse  purulent  expectoration  two  or  three  times  during 
the  twenty -four  hours  ;  this  will  gradually  grow  less  and  less 
in  quantity,  and  finally  cease  altogether  as  the  pleural 
cavity  becomes  obliterated. 

If  the  opening  takes  place  into  the  peritoneal  cavity, 
its  occurrence  is  usually  followed  by  a  rapidly  fatal  peri- 
tonitis. If  a  communication  is  established  with  the  in- 
testinal canal,  pus  will  appear  in  the  discharges  from  the 
bowels. 

When  the  patient  survives  the  establishment  of  an  open- 
ing, whether  it  be  external  or  internal,  spontaneous  or  arti- 
ficial, a  process  of  repair  at  once  commences  in  the  pleural 
cavity,  consisting  of  a  rapid  connective-tissue  formation, 
and  the  ordinary  contractions  attending  new  connective- 
tissue  developments  will  manifest  themselves ;  as  the  con- 
tents of  the  pleural  cavity  are  being  discharged,  retraction 
of  the  chest- wall  becomes  more  and  more  apparent,  and  dis- 
placement of  the  abdominal  and  thoracic  viscera  gradually 
takes  place, — this  process  is  necessarily  slow,  and  years 
may  elapse  before  it  is  completed. 

PHYSICAL  SIGNS. — The  physical  signs  of   empyema  are 


200  PHYSICAL   SIGNS. 

essentially  the  same  as  those  of  subacute  pleurisy, — except 
that  the  level  of  the  fluid  is  not  so  readily  changed  by  a 
change  in  the  position  of  the  patient.  If,  however,  by  the 
physical  signs  you  determine  the  presence  of  fluid  in  the 
pleura!  cavity  of  a  patient  very  much  debilitated,  who  has 
a  constant  cough  with  muco-purulent  expectoration,  hectic 
fever  with  profuse  sweats,  and  from  whose  history  little 
doubt  exists  but  that  the  fluid  accumulation  has  been  going 
on  for  a  long  time, — if,  after  observing  such  a  case  for  some 
time,  you  find  little  or  no  change  in  the  quantity  of  the 
fluid,  you  may  be  very  certain  that  the  fluid  in  the  pleural 
cavity  is  purulent.  The  only  way  to  reach  a  positive  diag- 
nosis is  to  withdraw  a  small  quantity  of  the  fluid  from  the 
pleural  cavity,  making  use  of  an  exploring-needle,  then 
submit  the  fluid  to  a  microscopical  examination,  and  it  will 
be  found  composed  principally  of  pus- cells. 

DIFFERENTIAL  DIAGNOSIS. — Unless  a  fistulous  opening 
exists,  a  positive  diagnosis  of  empyema  is  impossible,  ex- 
cept by  an  explorative  puncture  of  the  chest-walls.  When 
an  explorative  puncture  has  been  made,  and  some  of  the 
contents  drawn  off  and  subjected  to  a  microscopical  exami- 
nation, it  is  not  possible  to  confound  an  empyema  with 
any  other  thoracic  disease.  I  shall  not  therefore  detain 
you  with  any  questions  regarding  its  differential  diag- 
nosis. 

PROGNOSIS. — The  prognosis  in  empyema  is  always  bad. 
Statistics  show  that  among  empyemic  patients  in  whom 
spontaneous  openings  occur,  about  one  in  five  recover,  while 
among  those  in  whom  artificial  openings  are  established 
about  one-eighth  recover. 

These  patients  may  die  from  exhaustion  incident  to 
the  accumulation  of  a  large  quantity  of  pus,  or  from  ex- 
haustion which  attends  a  prolonged  and  abundant  puru- 
lent discharge.  Those  cases  which  occur  in  connection 
with  septicaemia  or  pygemia  are  always  fatal ;  while  those 
in  which  the  purulent  accumulation  is  slow  in  its  develop- 
ment, perhaps  the  result  of  a  sero-fibrinous  effusion,  may 
recover. 

In  this  disease,  the  judicious  use  of  the    aspirator  will 


CHEO^IC   PLEURISY.  201 

greatly  tend  to  render  the  prognosis  favorable.  During  the 
past  year,  I  have  seen  two  cases  make  a  complete  recovery, 
which  were  treated  by  early  and  repeated  aspiration. 

The  dangers  attending  a  perforation  of  the  diaphragm 
and  the  lung  have  been  already  sufficiently  described. 


COLLlEGlf   Olr 
l-K\  SIC  iMvi- 


LECTURE  XVII. 


PLEURISY. 

Chronic  Pleurisy  (continued). — Hydropneumothorax. — Hydrothorax. — Hiem- 

athorax. 

AT  the  close  of  my  last  lecture  I  had  reached  the  treat- 
ment of  empyema. 

In  the  treatment  of  this  affection  it  is  useless  to  attempt 
to  produce  absorption  of  the  purulent  accumulation ;  as 
soon  as  you  have  determined  that  a  pleural  cavity  contains 
pus,  its  removal  should  be  commenced  by  mechanical  means. 
At  your  first  aspiration  you  must  not  attempt  to  empty  the 
pleural  cavity  ;  remove  only  a  small  portion  of  the  accumu- 
lation, being  governed  in  the  performance  of  the  aspiration 
by  the  rules  which  I  have  already  given  you  for  the  removal 
of  serous  effusion.  Allow  from  three  to  six  days  between 
each  operation.  Imitate  as  far  as  possible  the  emptying  of 
a  pleural  cavity  by  a  spontaneous  opening,  that  is,  secure 
intermittent  discharges  and  draw  out  a  small  quantity  at 
each  operation.  It  is  impossible  to  perfectly  imitate  a  spon- 
taneous discharge,  for  that  would  necessitate  aspiration  far 
too  frequently.  At  each  aspiration  something  in  excess  of 
the  accumulation  which  has  taken  place  since  the  previous 
operation  should  be  removed.  The  rule  which  should  guide 
you  as  to  the  exact  quantity  of  fluid  to  be  removed  is,  never 
to  continue  its  removal  after  the  patient  feels  the  slightest 
uneasiness  or  constriction  in  breathing,  even  if  only  three  or 
four  ounces  have  been  removed  ;  this  rule  is  imperative.  If 
this  treatment  is  to  prove  successful,  after  a  time  you  will 
notice  that  retraction  of  the  chest-wall  is  taking  place.  If, 
at  each  successive  operation,  you  find  the  fluid  becoming 

-5rJ  HJJ 


CHRONIC   PLEUKISY.  203 

thinner  and  thinner,  your  prognosis  will  be  favorable ;  but 
if  the  fluid  becomes  thicker  and  emits  an  offensive  odor,  the 
prognosis  will  be  unfavorable. 

It  has  been  proposed,  when  large  accumulations  of  puru- 
lent fluid  have  been  rapidly  formed  in  the  pleural  cavity,  to 
make  a  permanent  opening  at  the  most  dependent  portion  of 
the  pleural  cavity,  sufficiently  large  to  permit  the  free  escape 
of  the  fluid.  In  those  forms  of  empyema  which  have  been 
described  as  occurring  in  connection  with  pyaemia,  sep- 
ticsemia,  and  certain  other  diseases,  unless  the  aspirator  is 
used  daily,  the  purulent  accumulation  will  exceed  in  quan- 
tity that  removed  by  the  aspirator.  Under  such  circum- 
stances, a  free  opening  through  the  chest- walls  is  warranted. 

The  objection  to  free  openings  into  the  pleural  cavity  in 
empyema  is,  that  the  entrance  of  air  into  the  cavity  will 
cause  the  purulent  accumulation  to  become  very  offensive, 
and  gangrene  of  the  pleura  is  very  liable  to  be  developed. 
To  a  certain  extent,  this  may  be  prevented  by  frequently 
washing  out  the  cavity  with  a  weak  solution  of  carbolic 
acid  or  some  other  disinfectant.  Experience  teaches  that 
very  few  persons  reach  complete  recovery  when  free  open- 
ings have  been  made  through  the  thoracic  wall  into  the 
pleural  cavity,  yet  this  procedure  is  warranted  in  the  class 
of  cases  already  referred  to. 

From  the  time  the  treatment  by  aspiration  is  commenced 
in  a  case  of  empyema,  every  possible  means  must  be  re- 
sorted to,  to  sustain  the  strength  of  the  patient.  He  must 
receive  the  most  nutritious  diet  with  a  moderate  amount  of 
stimulants.  Tonic  remedies,  such  as  quinine  and  iron,  are 
always  indicated,  and  cod-liver  oil  will  be  of  service  if  it  does 
not  interfere  with  the  stomach  digestion.  The  patient  must 
be  kept  in  the  open  air  as  much  as  possible,  and  a  change 
of  climate  is  often  attended  by  very  marked  improvement. 
It  must  be  remembered  that  the  reparative  processes  go  on 
most  rapidly  when  the  nutritive  processes  are  most  active. 

HYDROPNE  UMOTHORAX. 

I  will  pass  to  the  consideration  of  that  form  of  pleurisy 
to  which  I  gave  the  name  of  hydropneumothorax. 


204  MOEBID  ANATOMY. 

As  the  term  indicates,  this  is  a  condition  characterized  by 
the  presence  of  both  air  and  fluid  in  the  pleural  cavity. 
You  will  rarely  have  air  entering  the  pleural  cavity  without 
fluid  soon  following  its  entrance,  for  as  soon  as  air  enters 
the  cavity,  it  excites  inflammation  of  the  pleural  membrane, 
which  gives  pus  as  its  product. 

MORBID  ANATOMY. — The  morbid  changes  which  occur  in 
the  pleural  membrane,  and  in  the  pleural  cavity  in  hydro- 
pneumothorax,  very  nearly  correspond  to  those  described 
as  occurring  in  empyema.  The  changes  in  the  pleural 
membrane,  the  increase  of  tissue,  the  granular  appearance  of 
the  surface  of  the  pleura,  and  the  development  of  pus,  are 
similar.  By  the  entrance  of  air  into  the  pleural  cavity,  the 
lung  is  compressed  and  pushed  up  against  the  spinal  col- 
umn, in  the  same  manner  as  when  the  cavity  is  distended 
with  fluid.  The  quantity  of  fluid  varies  in  different  cases  ; 
at  one  time  the  cavity  will  be  nearly  filled  with  fluid  and 
contain  little  air, — again,  it  will  be  distended  with  air  and 
contain  little  fluid. 

When  extensive  and  firm  adhesions  of  the  pleural  sur- 
faces exist  prior  to  the  entrance  of  air  into  the  pleural 
cavity,  collapse  of  the  entire  lung  does  not  take  place,  but 
the  escaped  air  is  contained  in  a  small  space,  enclosed  by 
adhesions  on  all  sides.  This  condition  usually  is  present 
when  hydropneumothorax  is  developed  from  the  perfora- 
tion of  an  empyema. 

ETIOLOGY. — Regarding  the  formation  of  air  in  the  pleural 
cavity,  different  views  have  been  entertained.  Some  have 
claimed  that  gas  is  formed  in  the  pleural  cavity  as  a  secre- 
tion, in  the  same  manner  as  it  is  in  the  intestines  from  the 
mucous  membrane ;  such  a  result  is  possible,  but  by  no 
means  probable.  Again,  others  have  claimed  that  it  is  the 
product  of  decomposition  of  fluid  in  the  pleural  cavity  ; 
this  is  equally  improbable,  for  fluid  effused  into  cavities 
coated  with  a  lining  membrane,  resist  decomposition  in  a 
surprising  manner,  but  when  taken  from  such  cavities,  or 
exposed  to  air  in  the  cavity,  decomposition  rapidly  takes 
place.  Pus,  or  serum,  will  not  undergo  decomposition  in  a 
pleural  cavity,  so  long  as  it  is  not  exposed  to  air. 


HTDKOPXEUMOTHORAX,  205 

There  can  be  but  little  question  but  that  in  pneumotliorax 
and  hydropneumo thorax,  there  is  always  an  opening  from 
the  lung  outward  through  a  bronchial  tube  to  the  surface, 
or  from  the  surface  of  the  lung  inward  through  a  bronchial 
tube.  In  the  one  case,  the  ulcerative  process  commences 
within  the  lung-tissue,  and  in  the  other  it  commences  upon 
the  surface  of  the  lung.  In  rare  instances  air  enters  the 
pleural  cavity  in  connection  with  an  external  opening 
through  the  chest- wall.  In  most  cases  of  traumatic  pneu- 
motliorax. air  does  not  enter  the  pleural  cavity  through  the 
opening  in  the  chest-wall,  but  through  an  opening  in  the 
pulmonary  pleura,  for  the  lung  receives  injury  at  the  same 
time  that  the  opening  is  made  through  the  walls  of  the 
chest.  In  fracture  of  the  ribs  a  spicula  of  bone  sometimes 
perforates  the  pulmonary  pleura,  through  which  air  escapes 
from  the  lung  into  the  pleural  cavity,  and  gives  rise  to 
hydropneumothorax.  Entrance  of  air  into  the  pleural  ca- 
vity usually  occurs  either  in  connection  with  pulmonary 
phthisis,  gangrene  of  the  lung,  empyema,  or  pulmonary 
emphysema.  It  is  most  frequently  met  with  in  connection 
with  pulmonary  phthisis. 

The  destructive  processes  developed  in  the  lung  in  pul- 
monary phthisis  may  involve  a  bronchial  tube,  and  estab- 
lish a  communication  between  it  and  the  pleural  cavity. 

In  gangrene  of  the  lung  the  surface  of  the  organ  may  be 
involved,  and  with  a  rupture  of  the  pleura  air  will  escape 
into  the  pleural  cavity,  and  give  rise  to  the  changes  already 
referred  to. 

Again,  when  empyema  exists,  and  the  fluid  has  been  a 
long  time  in  the  pleural  cavity,  it  may  establish  an  opening 
through  the  lung  into  a  bronchial  tube,  thus  permitting  the 
fluid  to  be  expectorated,  and  air  to  enter  the  pleural  cavity. 

In  connection  with  pulmonary  emphysema,  a  sac  con- 
taining air  which  has  been  formed  upon  the  surface  of  the 
lung  ruptures  in  consequence  of  some  violent  effort  in 
coughing,  or  from  some  other  forced  inspiration,  and  air 
enters  the  pleural  cavity,  developing  pneumothorax,  and 
the  changes  which  it  will  produce  by  exciting  a  pleuritic 
inflammation  will  rapidly  develop  a  hydropneumothorax. 


206  SYMPTOMS. 

At  the  post-mortem  examination  of  one  who  has  died  of 
hydropneumo  thorax,  it  is  often  difficult,  and  sometimes 
impossible,  to  find  the  opening  in  the  pulmonary  pleura, 
!or  the  reason  that  in  some  instances  it  becomes  covered 
with  a  fibrinous  deposit,  and  in  others  the  opening  has 
been  closed  some  time  before  death  by  an  inflammatory 
process  in  the  lung-substance  at  the  point  of  the  opening. 

SYMPTOMS. — The  symptoms  which  attend  perforation  of 
a  lung  and  the  escape  of  air  into  a  pleural  cavity  are 
usually  well  marked,  but  they  are  somewhat  variable. 
First,  there  is  a  class  of  cases  in  which  the  symptoms  are 
severe  in  character :  the  patient  is  suddenly  seized  with 
an  intense  teazing  pain  in  the  side,  followed  by  hurried 
respiration  and  great  dyspnoea.  The  dyspnosa  is  extreme, 
comes  on  suddenly,  is  soon  followed  by  well-developed 
cyanosis  ;  the  patient  passes  rapidly  into  a  state  of  collapse, 
and  in  some  instances  death  occurs  in  a  few  hours. 

Usually,  however,  the  patient  survives  the  shock  of  the 
perforation,  and  after  a  time  becomes  comparatively  com- 
fortable, suffering,  however,  more  or  less  from  dyspnoea, 
unable  to  assume  a  recumbent  posture,  but  able  to  recline 
upon  the  affected  side.  As  the  pleural  cavity  becomes 
filled  with  the  fluid  effusion  which  results  from  the  attend- 
ing pleuritic  inflammation,  the  dyspnoea  and  cyanosis 
increase,  and  general  dropsy  gradually  develops.  It  is 
the  purulent  accumulation  in  the  pleural  cavity  which 
proves  fatal,  and  not  the  pneumothorax,  for  with  its  devel- 
ment  the  temperature  rises  and  the  patient  becomes  more 
manifestly  hectic,  if  hectic  has  previously  existed.  When 
the  purulent  accumulation  becomes  very  abundant,  the 
patient  dies  from  the  exhaustion  produced  by  the  intensity 
of  the  febrile  excitement,  or,  exhausted  by  the  fever,  dies 
from  collateral  congestion  and  oedema  of  the  opposite  lung. 

In  some  cases  the  symptoms  which  attend  the  entrance 
of  air  into  the  pleural  cavity  come  on  more  insidiously ; 
the  difficulty  of  breathing  may  be  gradually  developed, 
and  the  existence  of  air  in  the  pleural  cavity  may  not  be 
recognized  until  considerable  fluid  has  collected  in  the 
pleural  cavity.  When  pneumothorax  occurs  in  connec- 


HYDROPlSrEUMOTIIOKAX.  207 

tion  with  pulmonary  phthisis,  its  occurrence  is  marked 
by  very  active  symptoms ;  when  developed  in  connection 
with  pulmonary  emphysema,  its  development  is  very 
insidious. 

PHYSICAL  SIGNS. — The  physical  signs  of  hydropneumo- 
thorax  are  very  characteristic,  and  if  properly  appreciated 
will  always  enable  you  to  recognize  its  existence.  By 
inspection  you  will  notice  an  increase  in  the  size  of  the 
aifected  side,  with  bulging  of  the  intercostal  space,  which 
becomes  more  prominent  than  in  subacute  pleurisy ;  there 
will  be  the  displacement  of  viscera  seen  in  subacute 
pleurisy  when  the  pleural  cavity  is  distended  with  fluid, 
and  there  will  be  absence  of  motion  on  the  affected  side, 
while  upon  the  unaffected  side  the  respiratory  movement 
will  be  increased  in  force  and  frequency.  Upon  palpation 
you  will  find  that  there  is  entire  absence  of  vocal  fremitus 
upon  the  affected  side. 

Thus  far  you  will  have  found  no  difference  between  the 
physical  evidences  of  hydropneumothorax  and  subacute 
pleurisy. 

On  percussion,  when  the  patient  is  sitting  or  standing, 
there  will  be  tympanitic  resonance  from  the  summit  of  the 
affected  side  to  the  level  of  the  fluid ;  below  the  level  of  the 
fluid  there  will  be  complete  flatness.  As  in  subacute  pleu- 
risy, a  change  in  the  position  of  the  patient  will  change  the 
level  of  the  fluid. 

Upon  auscultation,  you  will  find  an  entire  absence  of  all 
respiratory  and  vocal  sounds  below  the  level  of  the  fluid ; 
but,  as  soon  as  you  reach  its  level,  if  the  opening  from  the 
bronchial  tube,  which  admits  the  air  into  the  pleural  cavity, 
still  remains  pervious,  amphoric  respiration  will  be  heard, 
and  it  will  be  metallic  in  character.  Metallic  tinkling  is  al- 
most uniformly  associated  with  amphoric  respiration,  and 
is  produced  in  a  variety  of  ways.  It  may  be  produced  by 
agitation  of  the  liquid  from  the  vibration  of  the  voice,  or  by 
coughing  and  full  inspiration,  or  by  dropping  of  liquid 
from  the  walls  of  the  cavity  upon  the  surface  of  the  fluid. 
It  is  more  frequently  produced  by  the  agitation  of  the  fluid 
from  speaking  and  coughing. 


208  DIFFERENTIAL   DIAGXC-SIS. 

The  characteristic  physical  sign  of  this  disease  is  the  suc- 
cussion  sound,  which  is  a  metallic,  splashing  sound,  pro- 
duced by  abruptly  shaking  the  chest  while  the  ear  is  rest- 
ing upon  its  surface. 

Over  the  affected  side  no  vesicular  breathing  can  be 
heard,  while  over  the  healthy  side  the  vesicular  breathing 
is  exaggerated. 

DIFFERENTIAL  DIAGNOSIS. — When  hydropneumothorax 
is  fully  developed,  it  is  scarcely  possible  to  confound  it 
with  any  other  disease,  but  it  is  possible  to  confound  pneu- 
mothorax  with  some  other  conditions.  As  I  have  already 
stated,  when  the  perforation  which  permits  the  entrance  of 
air  into  the  pleural  cavity  first  occurs,  the  only  physical 
evidences  of  its  occurrence  are  tympanitic  percussion, 
absence  of  all  respiratory  sounds  on  the  affected  side,  and 
intense  dyspnoea ;  the  same  development  of  signs  might 
occur  in  connection  with  complete  obstruction  of  a  large 
bronchus. 

Again,  it  is  said  that  pneumothorax  may  be  confounded 
with  extreme  pulmonary  emphysema.  Patients  suffering 
from  these  diseases  present  a  somewhat  similar  appearance ; 
in  both  classes  there  will  be  tympanitic  percussion,  but  in 
the  emphysematous  patient  the  tympanitic  percussion  will 
be  present  over  both  lungs,  while  in  a  patient  suffering  from 
pneumothorax  it  will  be  present  only  upon  the  side  on 
which  the  perforation  has  occurred.  In  emphysema  there 
will  also  be  heard  some  respiratory  sounds.  If  errors  in  the 
differential  diagnosis  of  these  two  conditions  are  possible, 
they  will  be  made  at  the  commencement  of  the  attack. 

A  large  cavity  in  the  lung-substance  may  be  mistaken  for 
hydropneumothorax.  I  have  never  met  with  a  pulmonary 
cavity  of  sufficient  size,  and  with  the  conditions  such  as  to 
produce  the  succussion  sound. 

Amphoric  respiration  and  metallic  tinkling  may  be  devel- 
oped in  a  large  cavity,  but  the  succussion  sound  will  be 
absent ;  but,  when  amphoric  respiration  and  metallic  tink- 
ling are  present  in  hydropneumothorax,  the  succussion 
sound  will  also  be  present. 

With  a  knowledge  of  the  history  of  the  patient,  and  a 


HYDKOPNEUMOTIIOKAX.  209 

proper  appreciation  of  the  physical  signs,  it  is  hardly  pos- 
sible for  you  to  confound  hydropneumothorax  with  any 
other  form  of  disease.  In  no  other  disease  are  the  physical 
signs  so  characteristic  and  unequivocal,  and  in  a  large  pro- 
portion of  cases  the  rational  symptoms  are  equally  diag- 
nostic. 

PROGNOSIS. — The  prognosis  in  hydropneumothorax  is 
always  unfavorable.  When  it  occurs  in  connection  with 
advanced  pulmonary  phthisis  or  gangrene,  it  generally 
proves  fatal  within  five  or  six  days. 

When  recovery  has  taken  place  in  cases  of  hydropneu- 
mothorax, either  they  have  been  of  traumatic  origin,  the 
result  of  great  muscular  strain  in  connection  with  extensive 
pulmonary  emphysema,  or  an  empyema  has  discharged 
itself  through  a  bronchus. 

There  is  record  of  a  few  recoveries  where  the  rupture 
occurred  in  the  early  stage  of  phthisis.  When  recovery 
does  take  place  it  is  reached  in  the  following  manner :  plas- 
tic material  is  poured  out  in  the  tissues  surrounding  the 
opening  in  sufficient  quantities  to  completely  close  them ; 
then  air  and  fluid  are  imprisoned  in  the  pleural  cavity,  the 
air  is  rapidly  disposed  of  by  the  pleural  membrane,  and  if 
the  closure  is  sufficiently  firm  to  be  retained  when  the  air 
has  been  removed,  the  case  will  be  changed  from  one  of 
hydropneumothorax  to  one  of  empyema. 

Cases  have  been  related  in  which  perforation  of  the  lung 
and  pneumothorax  were  present  without  any  fluid  collecting 
in  the  pleural  cavity.  Such  cases  are  of  such  rare  occur- 
rence that  they  can  hardly  be  taken  into  consideration  as 
regards  prognosis. 

TREATMENT. — The  treatment  of  this  affection  is  almost 
necessarily  palliative.  At  the  very  onset  of  the  attack,  when 
the  patient  is  suffering  from  the  shock  of  the  perforation,  a 
full  hypodermic  injection  of  morphine  will  be  found  of  ser- 
rice,  and  it  may  be  repeated  once  or  twice  a  day  for  the 
first  few  days.  If  the  patient  survives  the  first  few  days, 
stimulants  may  be  advantageously  administered,  and  he 
must  be  sustained  by  a  most  nutritious  diet. 

When  the  dyspnoaa  is  extreme  and  the  distress  of  the 

14 


210  SYMPTOMS. 

patient  very  great,  and  a  considerable  quantity  of  fluid  has 
accumulated  in  the  pleural  cavity,  the  question  will  arise, 
whether  a  free  opening  shall  be  made  through  the  chest- 
walls.  As  a  rule,  this  must  be  regarded  as  a  palliative 
measure,  and  should  be  resorted  to  only  in  extreme  cases. 
It  may  give  relief  for  a  time,  and  you  are  justified  in  re- 
sorting to  it  when  the  fluid  collection  is  abundant  and  the 
febrile  excitement  is  intense.  It  may  delay  the  fatal  ter- 
mination. 

HYDEOTHORAX. 

This  can  never  be  regarded  as  a  form  of  pleurisy,  although 
the  term  is  sometimes  incorrectly  employed  as  indicating 
the  presence  of  an  inflammatory  product  in  the  pleural 
cavity.  It  is  a  non-inflammatory  fluid  effusion  into  one  or 
both  pleural  cavities.  The  fluid  is  generally  clear,  of  a  yel- 
lowish color,  and  may  be  sufficient  in  quantity  to  compress 
to  a  considerable  degree  one  or  both  lungs. 

It  may  occur  in  any  chronic  exhausting  disease  whicn 
causes  general  hydrsemia. 

In  a  large  number  of  autopsies,  you  will  find  a  small 
amount  of  clear  or  bloody  serum  in  the  pleural  cavities, 
which  is  merely  the  result  of  post-mortem  changes ;  such 
conditions  should  not  be  regarded  as  evidence  of  hydro- 
thorax. 

SYMPTOMS. — Hydrothorax  usually  comes  on  insidiously, 
and  its  development  is  attended  by  no  febrile  symptoms. 
Its  occurrence  is  marked  by  steadily-increasing  dyspnoea, 
until  the  patient  reaches  a  condition  of  extreme  distress, — 
the  lips  become  livid,  the  finger-ends  blue,  and  the  respira- 
tion gasping.  He  is  unable  to  lie  down,  and  can  speak  only 
in  monosyllables.  On  physical  examination,  you  will  find 
the  signs  of  fluid  in  both  pleural  cavities. 

If  the  effusion  is  large,  the  action  of  the  heart  will  be  em- 
barrassed, as  shown  by  a  small,  feeble  pulse.  All  the  phe- 
nomena which  attend  this  condition  are  due  to  mechani- 
cal pressure  caused  by  the  presence  of  fluid  in  the  pleural 
cavities,  and  patients  die  cyanosed  as  the  result  of  dimin- 
ished breathing  capacity. 


HYDROTHORAX.  211 

Hydrothorax  generally  occurs  in  connection  with  general 
anasarca,  such  as  is  developed  in  Bright' s  disease,  or  it  may 
take  place  in  connection  with  any  disease  which  is  attended 
by  general  dropsy. 

DIAGNOSIS. — Ordinarily,  the  diagnosis  of  hydrothorax  is 
readily  made.  It  may  be  confounded  with  subacute  pleu- 
risy, but  generally  the  history  of  the  case  will  determine 
the  character  of  the  effusion.  Then,  its  simultaneous 
occurrence  on  both  sides,  in  connection  with  general 
dropsy,  without  any  irritant  or  attendant  fever,  will  be 
sufficient  to  enable  you  to  make  the  diagnosis  of  hydro- 
thorax. 

It  may  be  mistaken  for  pulmonary  oedema  :  the  two  con- 
ditions are  very  likely  to  occur  together ;  but,  in  pulmonary 
o?dema,  a  crackling  sound  will  be  heard  over  the  oadema- 
tous  lung,  which  sound  is  not  present  in  hydrothorax. 

The  physical  sign  of  hydrothorax  is  fluid  in  both  pleu- 
ral  cavities,  which  is  freely  movable  by  a  change  in  the 
position  of  the  patient,  and  is  not  attended  by  friction- 
sounds  nor  vocal  fremitus. 

PROGNOSIS. — The  danger  attending  hydrothorax  will  de- 
pend to  a  great  extent  on  the  general  condition  of  the  pa- 
tient at  the  time  of  its  occurrence. 

When  it  occurs  in  connection  with  general  anasarca  in 
Bright' s  disease,  or  in  extensive  heart-disease,  it  may  prove 
the  direct  cause  of  death. 

The  majority  of  cases  yield  readily  to  treatment. 

TREATMENT. — The  general  treatment  of  hydrothorax  cor- 
responds to  that  for  the  lemoval  of  dropsical  accumula- 
tions in  other  parts  of  the  body.  It  is  a  simple  dropsical 
effusion,  and  can  be  removed  by  the  administration  of  rem- 
edies which  diminish  the  quantity  of  water  in  the  blood. 
Such  remedies  are  the  hydragogue  cathartics,  diuretics, 
and  that  general  class  of  agents  employed  for  the  removal 
of  fluid  from  the  areolar  tissue.  In  many  cases  it  will  be 
impossible  to  wait  for  the  effects  of  diuretics  or  hydragogue 
cathartics,  as  the  patient  will  die  unless  immediate  relief  is 
afforded  from  the  pressure  of  the  fluid.  Under  such  cir- 
cumstances, the  aspirator  may  be  used  with  advantage, 


212  H^EMATHORAX. 

and  often  relief  is  obtained  by  the  removal  of  the  fluid 
from  the  pleural  cavity.  Those  remedies  may  be  employed 
which  are  of  service  in  the  treatment  of  general  anasarca. 

H^EMATHORAX. 

By  this  term  we  understand  the  escape  of  blood  into  the 
pleural  cavity. 

It  is  only  necessary  that  I  briefly  refer  to  its  causes  and 
symptoms,  for  it  is  never  a  primary  affection. 

The  escape  of  any  considerable  quantity  of  blood  into  the 
pleural  cavity  may  occur  in  connection  with  cancer  of  the 
lung  or  pleura,  from  the  bursting  of  an  aneurism,  the  rup- 
ture of  the  pleura  resulting  from  an  extensive  pulmonary 
apoplexy  and  escape  of  blood  from  the  lung,  and  the  rup- 
ture of  a  vessel  from  injury.  Sometimes  blood  is  mixed 
with  pleuritic  effusion,  the  product  of  pleuritic  inflamma- 
tion in  those  of  a  scorbutic  or  purpuric  diathesis. 

The  symptoms  of  hsemathorax  are  those  of  liquid  accu- 
mulation in  the  pleural  cavity,  with  the  accompanying  evi- 
dences of  internal  hemorrhage. 

In  those  cases  where  there  is  no  appreciable  traumatic 
cause  for  the  bleeding,  all  that  can  be  done  is  to  keep  the 
patient  at  rest. 

In  some  instances  relief  may  be  obtained  by  the  perform- 
ance of  paracentesis. 


LECTURE  XVIII. 


PULMONAEY  PHTHISIS. 

Catarrhal  Phthisis. — Morbid  Anatomy. — Fibrous  Phthisis. — Morbid  Anatomy. 
— Tubercular  Phthisis. — Morbid  Anatomy. 

WE  pass  from  the  different  forms  of  pneumonia  and 
pleurisy,  which  have  been  engaging  our  attention,  to  pul- 
monary phthisis. 

Whatever  view  may  be  entertained  as  to  the  exact  nature 
of  phthisis  in  all  its  forms,  inflammation  must  be  regarded 
as  the  great  element  of  destruction.  There  can  be  no  ques- 
tion but  that  the  principal  anatomical  changes  which  occur 
in  the  lungs  of  one  who  has  died,  giving  the  history  and 
symptoms  of  pulmonary  phthisis,  are  inflammatory  in  their 
character.  At  the  present  time,  perhaps,  there  is  no  subject 
within  the  whole  range  of  practical  medicine,  concerning 
which  competent  observers  differ  so  widely,  as  the  interpre- 
tation of  the  anatomical  facts  of  pulmonary  phthisis;  all 
agree  as  to  the  microscopical  appearances  presented  by  lung- 
tissue  which  is  the  seat  of  phthisical  changes ;  but  in  the 
interpretation  of  these  appearances  they  differ  very  widely. 

One  class  of  observers  maintain  that  the  deposit  and  ulti- 
mate breaking  down  of  tubercle  in  the  lungs  is  the  essential 
anatomical  element  of  this  disease  ;  while,  on  the  other  hand, 
another  class  of  observers  find  nothing  in  these  anatomical 
changes  which  cannot  be  properly  classed  under  the  head  of 
inflammatory  changes. 

While  I  recognize  the  fact  that  there  is  great  difficulty  in 
drawing  the  line  of  distinction  between  what  is  commonly 


214  DIVISIONS. 

termed  tubercle  and  certain  well-recognized  inflammatory- 
tissue  changes,  I  am  disposed  to  the  opinion  that  there  is 
nothing  any  more  specific  about  pulmonary  phthisis  than 
there  is  about  chronic  parenchymatous  nephritis,  and  that 
the  varying  proportions  in  which  the  different  types  of  in- 1 
flammatory  changes  exist  in  different  cases,  combined  with ' 
their  different  stages  of  evolution,  account  for  the  varying 
appearances  presented  by  lungs  in  one  case  of  phthisis  as 
compared  with  lungs  in  another. 

It  seems  to  me  that  we  have  reached  this  point  with  re- 
gard to  the  anatomical  changes  of  pulmonary  phthisis,  viz. : 
that  all  these  changes,  call  them  tubercular  if  you  choose, 
can  be  arranged  under  the  head  of  inflammation  ;  and  that 
they  only  differ  according  to  the  primary  seat  and  character 
of  the  inflammatory  process. 

In  one  class  of  cases  the  primary  changes  are  in  the  cavi- 
ties of  the  alveoli  and  bronchi,  and  are  epithelial  and  cellu- 
lar in  their  nature. 

In  another  class  of  cases  the  primary  changes  occur  in 
the  bronchial  and  alveolar  connective  tissue.  These  connec- 
tive-tissue hyperplasias  may  be  nodular,  linear,  or  massive ; 
they  may  occur  in  lung-tissue  that  has  already  undergone  a 
change  of  the  epithelium  in  the  air-cells,  or  they  may  occur 
as  an  independent  development. 

Again,  in  still  another  class  of  cases,  the  primary  changes 
may  occur  in  the  lymphoid  elements  of  the  lung.  Hyper- 
plasia  of  the  lymphoid  elements  is  almost  always  associated 
with  connective-tissue  hyperplasia,  and  the  little  masses  or 
nodules  formed  as  the  result  of  these  two  changes  have  all 
the  anatomical  characters  of  what  are  ordinarily  termed 
tubercles ;  it  is  certainly  impossible  with  the  microscope  to 
distinguish  one  from  the  other. 

Perhaps  all  of  these  anatomical  changes  may  be  found  in 
a  single  lung ;  but  in  every  instance  a  careful  examination 
of  the  diseased  structure  will  determine  which  of  these  pro- 
cesses was  the  primary  element  in  the  pathological  changes. 
The  tendency  of  all  these  morbid  processes  is  to  pulmonary 
consolidation  and  to  advancing  destruction  of  the  respira- 
tory organs. 


PULMONARY  PHTHISIS.  215 

For  the  sake  of  convenience  in  studying  this  subject,  I 
'shall  divide  phthisis  according  to  its  most  marked  anatom- 
,ical  lesions  into  three  varieties  : 

CATARRHAL  PHTHISIS, 
FIBROUS  PHTHISIS, 
TUBERCULAR  PHTHISIS. 

It  should  be  remembered  that  these  three  forms  may 
occur  either  separately  or  together. 

I  shall  first  describe,  as  briefly  as  possible,  the  anatomical 
changes  of  catarrhal  phthisis. 

CATARRHAL   PHTHISIS. 

MORBID  ANATOMY. — As  we  study  the  morbid  processes 
of  this  variety  of  phthisis,  you  will  readily  see  that  it  is 
nothing  more  nor  less  than  a  chronic  catarrhal  or  cheesy 
pneumonia,  which,  although  it  differs  somewhat  in  its  mor- 
bid anatomy  from  acute,  like  the  acute,  is  almost  invariably 
preceded  by  catarrh  of  the  bronchial  mucous  membrane. 
This  catarrh  usually  manifests  itself  in  the  bronchial  tubes 
which  ramify  the  upper  lobes  of  the  lungs.  Why  these  tubes 
are  the  seat  of  this  form  of  bronchial  catarrh,  I  do  not  know, 
but  observation  has  shown  that  such  is  the  fact.  It  differs 
from  all  other  bronchial  catarrhs  in  its  persistence  and  in  its 
tendency  to  recur,  as  well  as  in  the  abundance  of  cells  (which 
are,  for  the  most  part,  changed  epithelial  cells)  to  be  found 
in  the  inflammatory  products.  These  cells  render  it  so 
tenacious  that  it  adheres  closely  to  the  bronchial  walls, 
from  which  it  is  removed  with  difficulty,  its  removal  caus- 
ing frequent  and  violent  paroxysms  of  coughing. 

This  catarrh  gradually  extends  from  the  larger  to  the 
smaller  bronchi,  until,  finally,  it  reaches  the  ultimate  tubes  ; 
these  become  so  completely  obstructed  by  the  inflammatory 
products,  that  the  passage  of  air  to  the  air-vessels  beyond 
is  prevented,  and,  as  a  result,  the  alveoli  beyond  the  point 
of  obstruction  collapse ;  following  the  collapse,  epithelial 
desquamation  occurs  in  the  alveoli,  together  with  inflam- 
matory infiltration  of  the  alveolar  walls.  In  some  instances 
the  epithelial  desquamation  extends  directly  from  the  small 


216  MORBID    ANATOMY. 

bronchi  to  the  alveoli.  In  either  case  the  result  is  the 
same ;  the  lobules  supplied  by  the  obstructed  or  inflamed 
bronchi  become  distended  with  cells,  which  rapidly  under- 
go fatty  metamorphosis. 

The  pneumonia  which  is  thus  developed  is  exceedingly 
slow  in  all  its  processes  :  passing  through  the  stages  of  con- 
gestion and  oedema,  it  finally  reaches  a  stage  of  complete 
hepatization,  after  which  it  may  entirely  resolve,  and  leave 
no  trace  behind  it ;  or,  after  reaching  the  stage  of  hepatiza- 
tion, the  contents  of  the  alveoli  may  become  fatty,  and 
undergo  a  process  of  dry  degeneration,  and  become  con- 
verted into  a  firm,  dry,  caseous  mass,  constituting  what  is 
called  cheesy  pneumonia. 

Let  us,  for  a  moment,  examine  a  little  more  in  detail  these 
morbid  processes.  Starting  with  the  changes  in  the  small- 
er bronchi,  we  find,  after  the  bronchi  have  become  com- 
pletely filled  with  inflammatory  products,  that  these  pro- 
ducts become  cheesy,  and  the  nutrition  of  the  walls  of  the 
tubes  at  the  point  of  obstruction,  from  the  pressure  of  the 
cheesy  plug,  becomes  somewhat  interfered  with,  and  the 
walls  attenuate,  or  a  peribronchitis  may  be  developed,  and 
fibrous-tissue  increase  may  take  place  at  the  points  of  ob- 
struction. At  the  post-mortem  examination  these  points 
will  present  a  gross  appearance,  resembling  what  has  been 
called  tubercle.  Again,  at  the  points  of  bronchial  obstruc- 
tion, a  process  of  ulceration  may  at  any  time  be  estab- 
lished ;  we  then  find  a  sharply  defined  shallow  loss  of 
substance,  not  only  of  the  bronchial  walls,  but  of  the  adja- 
cent lung-substance. 

At  the  same  time  that  these  changes  have  been  taking 
place  in  the  bronchi,  the  lobules  which  are  connected  with 
them  have  also  become  distended  with  cells,  which  have 
become  fatty,  and  perhaps  cheesy.  We  have,  then,  not 
only  a  cheesy  nodule  in  the  bronchial  tube  presenting  the 
appearance  of  so-called  yellow  tubercle,  but  we  have  also  a 
cheesy  nodule  produced  in  the  lobule,  having  the  appear- 
ance of  a  yellow  tubercle  of  larger  size.  While  these, 
changes  are  going  on,  more  or  less  connective-tissue  increase 
takes  place  around  the  cheesy  mass. 


PULMONARY  PHTHISIS.  217 

If  only  a  few  lobules  are  the  seat  of  these  changes,  the 
cheesy  nodule  may  become  encapsulated,  and  the  patient 
completely  recover ;  yet  there  now  exists  a  predisposing 
cause  to  another  bronchitis  of  the  same  character,  which 
follows  the  same  general  course  as  the  preceding  one  ;  other 
nodules  will  become  cheesy  in  the  same  manner,  and  a  still 
larger  cheesy  nodule  will  be  formed,  which  also  may  be- 
come encapsulated.  This  process  may  be  repeated  several 
times  before  an  attack  of  bronchitis  will  occur  which  shall 
go  on  to  extensive  destruction  of  lung-tissue. 

As  a  general  rule,  recovery  is  made  from  two  or  three 
attacks  of  bronchial  catarrh,  which  leave  behind  them 
cheesy  nodules.  It  is  possible  for  resolution  to  occur  in 
a  cheesy  nodule  after  the  manner  described  as  taking  place 
in  acute  catarrhal  pneumonia,  and  the  aifected  portion  of 
lung  to  resume  its  normal  condition :  this  result  is  rarely 
reached  if  the  cheesy  nodule  is  of  large  size  ;  usually,  if  the 
removal  of  the  cheesy  material  takes  place,  either  by  ex- 
pectoration or  absorption,  the  affected  air-cells  are  obliter- 
ated by  the  contraction  of  the  new  connective  tissue. 

The  amount  of  lung-tissue  which  undergoes  cheesy  hepat- 
ization  in  the  course  of  a  catarrhal  phthisis  varies  very 
much ;  a  large  portion  of  a  lobe  may  become  cheesy,  or 
large  cheesy  masses  may  be  scattered  here  and  there  through 
^he  lung,  or  the  lung  may  be  studded  with  a  large  number 
of  small  yellow  nodules,  varying  in  size  from  a  pin'  s-head 
to  that  of  a  pea  ;  the  lung- tissue  between  them  is  at  some 
points  normal,  at  others  anaemic,  and  still  at  others  hyper- 
semic  and  oadematous.  These  cheesy  masses  were  formerly 
termed  crude  tubercle — the  larger  masses  were  called  yellow, 
opaque,  infiltrated  tubercle  ;  the  smaller  were  called  miliary 
tubercle. 

As  I  have  already  stated,  these  cheesy  nodules  may 
undergo  resolution,  soften,  and  be  expectorated,  and  the 
affected  lung-tissue  return  to  its  normal  condition ;  or,  if 
they  are  of  small  size,  they  may  become  calcareous  and  en- 
capsulated. A  far  more  frequent  termination  of  cheesy 
pneumonia  is  the  softening  of  the  caseous  nodules,  and  the 
formation  of  cavities. 


218  MOKBID   AXATOMY. 

The  length  of  time  which  a  cheesy  nodule  may  remain 
unchanged  in  the  lung,  depends  partly  upon  its  size  and 
partly  upon  the  rapidity  of  its  formation ;  the  larger  the 
size,  and  the  more  rapid  its  formation,  the  greater  the 
danger  of  softening  and  the  formation  of  a  cavity.  Ordi- 
narily, a  cheesy  nodule  attains  the  size  of  a  hazel-nut  before 
it  softens ;  but  a  single  lobule,  if  it  has  rapidly  become 
cheesy,  will  soften  as  soon,  or  sooner,  than  a  large  nodule 
that  has  slowly  become  cheesy ;  with  the  softening  of  the 
caseous  material,  the  alveolar  walls  lose  their  vitality,  dis- 
integrate, and  cavities  are  formed.  A  communication  is 
established  between  cavities  thus  formed  and  the  bronchial 
tubes,  by  an  ulcerative  process  which  usually  commences 
in  the  tubes  ;  sometimes  a  cavity  formed  by  lobular  soften- 
ing simply  enlarges  a  cavity  already  formed  by  a  bronchial 
dilatation.  In  many  instances  the  softening  process  com- 
mences on  the  surface  of  the  cheesy  nodule,  and  as  the 
walls  of  the  alveoli  are  broken  down,  the  ultimate  bronchial 
tubes  leading  to  the  cheesy  nodules  share  in  the  same 
destruction ;  consequently,  shreds  of  elastic  lung-tissue  and 
bronchial  tissue  appear  in  the  expectoration,  demonstrating 
that  both  lung-tissue  and  bronchial  tubes  are  involved  in 
the  destructive  process.  It  is  not  altogether  unfrequent 
that  the  process  of  softening  and  ulceration  goes  on  so 
rapidly,  that  it  assumes  the  character  of  gangrene.  Before 
this  destructive  process  reaches  excavation,  a  conservative 
inflammatory  process  is  established  in  the  pulmonary  con- 
nective tissue,  corresponding  to  that  already  described 
under  the  head  of  interstitial  pneumonia.  This  conserva- 
tive process  is  in  operation  prior  to  the  process  of  softening, 
but  when  the  softening  process  commences,  it  goes  on  more 
rapidly  until  connective-tissue  indurations  are  formed 
throughout  the  affected  portion  of  lung ;  on  the  one  hand 
it  is  connected  with  the  thickened  pleura,  and  on  the  other 
with  the  peribronchial  and  perivascular  connective-tissue 
sheaths.  The  cavities,  which  result  from  the  destructive 
processes  already  described,  are  separated  from  each  other 
by  masses  of  fibrous  tissue. 

The  connective  tissue,  when  once  formed,  gradually  con- 


PULMONARY   PHTHISIS.  219 

tracts  and  occupies  less  space  than  the  lung-tissue  which  it 
replaces ;  as  it  shrinks,  the  thoracic  walls  fall  in  over  the 
affected  portion  of  lung. 

The  development  of  fibrous  pneumonia,  in  connection  with 
the  pathological  processes  of  chronic  cheesy  pneumonia, 
must  always  be  regarded  as  a  necessary,  but,  in  some 
respects,  a  conservative  process. 

When  the  process  of  softening  is  rapid,  and  the  patient 
dies  of  acute  catarrhal  phthisis,  very  little  fibrous  indura- 
tion will  be  found.  The  cavities  which  form  in  the  lungs  in 
catarrhal  phthisis  increase  in  size  by  peripheral  disintegra- 
tion, or  by  small  cavities  coalescing.  The  contents  of  the 
cavities  will  vary  with  the  rapidity  of  the  destructive  pro- 
cesses. 

I  will  now  pass  to  the  history  of  the  anatomical  changes 
of  fibrous  phthisis. 

FIBROUS  PHTHISIS. 

Under  the  head  of  interstitial  pneumonia,  I  have  given 
you  a  history  of  the  principal  anatomical  changes  which 
occur  in  this  form  of  phthisis.  It  may  be  associated  with 
slight  catarrhal  pneumonias,  in  which  desquamation  of  the 
alveolar  epithelium  and  hyperplasia  of  the  pulmonary  con- 
nective tissue  are  the  only  or  principal  pathological  pro- 
cesses. It  may  occur  in  small  nodules,  or  involve  an  entire 
lobe.  It  is  usually  accompanied  by  peribronchitis  and 
bronchiectasis. 

MORBID  ANATOMY. — A  section  of  a  portion  of  lung  that 
is  the  seat  of  this  form  of  phthisis  presents  a  smooth  or  gran- 
ular surface,  or  has  a  striated  appearance,  as  if  interwoven 
with  fibrous  elements.  When  granular,  the  granules  are 
composed  of  imperfect  rounded  cells,  and  each  granule  is 
set  in  the  midst  of  a  hyperplasia  of  connective  tissue  ;  they 
are  not  tubercles,  but  connective-tissue  hyperplasias.  This 
newly  formed  tissue  contains  more  or  less  dark  pigment 
matter  which  gives  to  the  cut-surface  a  bluish  or  gray  color. 
If  the  process  is  old,  the  lung  will  be  tough,  but  if  the  pro- 
cess is  recent,  the  leather-like  toughness  is  not  so  manifest. 

The  microscope  will  show  the  indurated  tissue  to  be  made 


220  MORBID   ANATOMY. 

up  of  cell-elements  in  various  stages  of  development  on  a 
highly  organized  fibrous  tissue. 

The  connective-tissue  hyperplasia  which  occurs  in  con- 
nection with  this  form  of  phthisis  may  commence  in  the 
inter-cellular  tissue  around  the  blood-vessels,  or  extend  into 
the  lung- tissue  from  the  pleura ;  it  may  also  commence  in 
the  walls  of  the  air-cells,  and  in  the  connective-tissue  sheaths 
of  the  terminal  bronchi.  The  pleura  over  the  indurated 
lung-tissue  is  thickened,  sometimes  to  the  extent  of  half  an 
inch.  When  the  indurating  process  has  existed  for  some 
time,  the  apex,  and  in  some  instances  the  whole  lung,  is  con- 
verted into  tough  fibrous  tissue,  all  traces  of  normal  lung- 
tissue  being  obliterated. 

Within  this  fibrous  mass  the  bronchi  present  various  con- 
ditions; their  walls  at  one  point  are  thickened  and  their 
calibre  diminished,  while  at  another  they  are  thinned  and 
dilated.  The  dilatations  may  be  cylindrical,  fusiform,  or 
sacculated,  and  are  generally  most  numerous  at  the  apex  of 
the  affected  lung,  although  you  will  sometimes  find  an  en- 
tire lung  studded  with  small  bronchial  cavities,  separated 
from  each  other  by  thick  bands  of  fibrous  tissue  ;  these  cav- 
ities have  for  the  most  part  a  thin  membranous  lining,  which, 
on  careful  examination,  will  be  found  to  be  continuous  with 
the  mucous  lining  of  the  bronchi,  and  this  will  establish  the 
fact  that  they  are  bronchial  dilatations  which  are  always 
accompanied  by  more  or  less  peribronchitis.  Sometimes  in 
these  cavities  we  find  masses  which  present  the  appearance 
of  cheesy  nodules,  but  they  are  simply  secretions  which 
have  accumulated  in  the  cavities.  Not  unfrecjuently,  these 
cavities  contain  a  material  which  has  an  offensive  odor  ;  this 
is  nothing  more  than  a  secretion  from  the  cavity  which  has 
undergone  decomposition. 

The  portion  of  lung  which  is  the  seat  of  fibrous  phthisis 
will  vary  in  color  according  to  the  amount  of  pigmentation 
which  it  has  undergone  :  when  this  is  considerable,  the  lungs 
will  be  of  a  black  or  dark  color ;  it  is  this  which  has  given 
rise  to  the  term  black  phthisis.  The  same  appearance  in 
color  may  be  met  with  in  the  lungs  of  those  who  work  in 
coal-mines  and  places  of  like  character. 


PULMONARY  PHTHISIS.  221 

I  will  now  pass  to  the  consideration  of  that  form  of  phthi- 
sis to  which  has  been  given  the  name  tubercular,  a  variety 
not  frequently  met  with. 

TUBERCULAR  PHTHISIS. 

Recent  researches  have  tended  to  bring  tuberculosis  into 
the  category  of  infectious  diseases.  I  shall  discuss  the  sub- 
ject of  tubercle  only  so  far  as  it  is  connected  with  pulmonary 
consolidation  attended  by  a  phthisical  history,  and  shall 
leave  the  question  of  its  infectious  or  non-infectious  nature 
to  be  established  by  future  studies.  I  am  not  prepared  to 
say  it  is  or  is  not  necessary  that  there  should  be  a  cheesy 
nodule  prior  to  the  development  of  tubercle,  but  I  am 
strongly  inclined  to  the  opinion  that  tubercles  should  be 
included  among  inflammatory  growths. 

Many  competent  observers  favor  the  opinion  that  those 
bodies  which  have  been  called  miliary  tubercles,  and  which 
have  been  found-  in  the  lungs  of  patients  who  have  died 
with  the  symptoms  of  phthisis,  are  nothing  more  nor  less 
than  lymphoid  and  connective-tissue  hyperplasias. 

MORBID  ANATOMY. — In  lungs  that  are  the  seat  of  tuber- 
cular phthisis,  you  will  find,  scattered  more  or  less  abun- 
dantly throughout  the  substance,  small,  grayish,  semi-trans- 
parent granulations  ;  or  a  portion  of  lung  may  be  infiltrated 
with  these  granulations,  which  will  give  to  it  a  gelatinous 
appearance.  These  granules  are  composed  of  lymphoid 
cells,  held  together  by  a  network  of  hyaline  connective 
substance ;  they  cannot  be  distinguished  from  lymphoid 
outgrowths.  They  originate  in  part,  if  not  altogether,  from 
tissues  belonging  to  the  lymphatic  system,  especially  from 
the  lymphatic  sheaths  of  the  small  arteries,  and  in  the  mi- 
nute masses  of  adenoid  tissue  which  exist  in  the  immediate 
vicinity  of  the  bronchioles,  or  in  the  walls  of  the  alveoli. 
In  their  development  the  lymphoid  cells  multiply  at  sepa- 
rate centres  around  the  blood-vessels,  and  thus  numerous 
miliary  nodules  are  produced,  which,  as  they  increase, 
gradually  compress,  and  ultimately  may  entirely  occlude 
the  vessel,  or  they  cause  a  diminution  in  the  calibre  of  the 
bronchioles,  and  thickening  of  the  alveolar  walls.  This  oc- 


222  MORBID  ANATOMY. 

elusion  of  the  small  vessels  is  characteristic  of  what  is 
termed  tubercular  growths.  (In  the  solid  viscera,  tubercles 
are  found  in  the  course  of  the  lymphatic  channels. ) 

These  lymphoid  growths  are  best  observed  and  studied 
in  the  lungs  of  children  when  they  are  the  seat  of  tuber- 
cular phthisis.  In  most  cases,  these  granules  originate  from 
cells  situated  within  the  lymphatic  vessels  ;  wherever  they 
occur,  they  are  structurally  inseparable  from  the  tissue  in 
which  they  grow ;  some  have  regarded  these  nodules  as 
connective-tissue  hyperplasias. 

Soon  after  these  nodules  are  formed  they  undergo  rapid 
anaemic  necrosis,  which  commences  in  their  contents,  and 
consists  of  fatty  metamorphosis  and  atrophy  of  their  cel- 
lular elements,  after  which,  within  the  surrounding  tissues 
which  have  participated  in  their  growth,  they  form  a  cheesy 
mass. 

Formerly,  when  they  reached  a  caseous  condition,  they 
were  called  yellow  tubercle ;  but  this  condition  is  merely 
a  stage  of  the  retrogressive  process ;  afterward  they  may 
soften,  or  dry  up  into  a  firm  horn-like  mass.  When  they 
become  aggregated  and  cheesy,  it  is  difficult,  by  their  gross 
appearance,  to  distinguish  them  from  miliary  cheesy  nodules 
of  catarrhal  phthisis. 

Usually,  with  these  nodular  developments,  cellular  forma- 
tions take  place  in  the  air-cells  of  the  adjoining  lung-tissue, 
similar  to  those  which  have  been  described  as  taking  place 
in  the  epithelial  form  of  catarrhal  pneumonia,  and  if  these 
diseased  processes  are  slow  in  their  progress,  the  connective 
tissue  of  the  affected  portion  of  lung  is  increased  in  a  man- 
ner similar  to  that  described  as  characterizing  interstitial 
pneumonia  ;  these  processes  combined,  seem  to  infiltrate 
and  consolidate  the  parenchyma  of  the  lung.  As  the 
diseased  process  progresses,  the  tubercular  and  catarrhal 
nodules  coalesce,  the  alveolar  walls  disappear,  each  nodule 
softens,  and  disintegration  goes  on  until  a  cavity  is  formed, 
and  a  communication  established  with  a  bronchus. 

During  the  destructive  process  which  follows  the  casea- 
tion  of  these  nodules,  the  same  indurating  processes  take 
place  in  the  affected  portion  of  lung  which  have  already 


PULMOFAKT  PHTHISIS.  223 

been  described  in  connection  with,  the  morbid  changes  of 
catarrhal  phthisis. 

When  consolidation  of  the  affected  portion  of  lung  is 
reached,  as  the  result  of  these  combined  processes,  there  are 
always  two  elements  present — the  catarrhal  element  in  the 
air-cells,  and,  mingled  with  it,  a  thickening  of  the  al- 
veolar walls,  or  an  outgrowth  upon  the  sheaths  of  the 
blood-vessels,  or  along  the  bronchial  tubes,  of  adenoid  or 
lymphoid  bodies.  The  evidences  of  catarrhal  pneumonia 
are  constant ;  the  alveolar  walls  are  also  thickened  by  the 
nodular  outgrowths  which  considerably  diminish  the  calibre 
of  the  alveoli.  The  catarrhal  elements  in  the  alveoli  usually 
undergo  rapid  degenerative  changes,  become  cheesy,  and 
when  this  occurs,  being  surrounded  by  alveolar  walls  which 
are  in  a  condition  far  less  able  to  resist  these  degenerative 
changes  than  are  normal  alveolar  walls,  as  soon  as  the 
softening  process  succeeds  the  cheesy,  the  alveolar  walls 
give  way,  and  cavities  are  rapidly  formed. 

Briefly  given,  these  are  the  characteristic  anatomical 
changes  of  tubercular  phthisis  ;  at  a  glance  you  are  able  to 
recognize  the  fact  that  there  is  a  marked  difference  in  the 
morbid  anatomy  of  the  three  forms  of  phthisis  to  which  I 

,ve  referred. 

In  the  first  instance  we  have  primarily  and  principally  a 
atarrhal  process  ;  in  the  second,  a  fibrous  process  ;  in  the 

ird,  the  primary  changes  are  in  the  lymphatics  of  the  lungs. 

ese  three  processes  may  all  be  present  in  the  same  lung. 
We  may  have  a  catarrhal  and  fibrous,  a  tubercular  and 
catarrhal,  and,  if  the  tubercular  continues  for  a  sufficient 
length  of  time,  a  tubercular,  catarrhal,  and  fibrous.  Al 
though  all  these  forms  of  phthisis  may  be  present  in  the  same 
lung,  in  most  instances  it  is  possible  to  determine  which  has 
been  the  primary  and  leading  process. 

At  your  post-mortem  examination  of  those  who  have  died 
presenting  the  symptoms  of  acute  or  chronic  phthisis,  the 
most  constant  and  prominent  morbid  change  will  be  pul- 
monary consolidation,  which  may  be  due  to  cheesy  pneumo- 
nia, fibrous  induration,  or  tubercle,  or  all  these  combined. 

At  a  later  stage  of  the  process,  in  addition  to  the  above 


224  MOEBID   ANATOMY. 

you  will  find  cavities  of  various  sizes,  containing  a  great 
variety  of  elements,  between  which  and  around  which  will 
be  found  indurated  lung-tissue  and  cheesy  masses  ;  some- 
times the  cavities  will  have  a  well-formed  lining  membrane, 
and  contain  pus,  while  at  other  times  their  walls  will  be 
ragged,  and  contain  pus,  cheesy  matter,  and  broken-down 
lung-tissue,  and  oftentimes  this  will  be  of  an  offensive  char- 
acter. 

The  bronchi  will  also  exhibit  a  great  variety  of  morbid 
changes.  Many  of  the  minute  tubes  which  traverse  the  con- 
solidated lung- tissue  will  be  found  obliterated,  others  will 
be  dilated  into  cavities  of  considerable  size  at  some  points, 
and  at  others  they  will  be  contracted,  and  their  walls  hyper- 
trophied.  Within  the  cavities  formed  by  the  bronchial 
dilatation  there  will  be  found  purulent  and  exudative  mate- 
rial, and  sometimes  cheesy  nodules  ;  sometimes  ulcerations 
of  the  bronchi  will  be  found. 

Where  the  bronchial  tubes  have  suffered  no  structural 
change,  they  are  the  seat  of  a  catarrh  which  furnishes  a  se- 
cretion rich  in  cells  ;  this  bronchial  catarrh  is  the  main  source 
of  expectoration  in  phthisical  subjects. 

The  blood-vessels,  especially  the  bronchi  of  the  pulmonary 
artery,  in  the  consolidated  lung-tissue,  are  found  more  or 
less  obliterated.  In  the  walls  of  cavities,  the  obliterated  ves- 
sels often  form  prominent  ridges  ;  sometimes  they  stretch 
from  one  wall  of  the  cavity  to  the  other,  in  the  form  of  liga- 
ments. 

Whenever  the  structural  changes  in  the  pulmonary  sub- 
stance reach  the  surface  of  the  lungs,  the  pleura  becomes 
thickened  and  the  two  surfaces  more  or  less  adherent ;  the 
apex  of  the  lung  is  often  covered  with  a  thick  fibrinous 
mass,  the  pleural  sac  being  entirely  obliterated. 

This  increase  in  the  pleural  tissue  may  undergo  cheesy  or 
cretaceous  transformation. 

In  a  small  proportion  of  cases,  in  connection  with  these 
changes,  tubercular  nodules  will  be  seen  scattered  through- 
out the  substance  and  on  the  pleural  surfaces  of  the  lungs. 

I  have  already  shown  that  the  primary  or  principal  ana- 
tomical changes  which  take  place  in  the  parenchyma  of 


PULMONARY   PHTHISIS.  225 

the  lungs,  in  the  different  varieties  of  pulmonary  phthisis, 
have  their  seat  in  the  bronchi. 

In  catarrhal  phthisis,  a  purulent  peribronchitis  precedes 
the  alveolar  changes,  and  leads  to  the  development  of  yellow, 
purulent,  and  cheesy  masses,  and  to  lobular  infiltration  and 
necrosis. 

In  fibrous  phthisis,  nodular  or  disseminated  peribronchitis 
is  often  the  primary  seat  of  the  connective-tissue  develop- 
ments. 

In  tubercular  phthisis,  the  development  of  the  miliary 
nodules  in  the  walls  of  the  bronchi  is  attended  by  more  or 
less  extensive  peribronchitis,  which  may  be  either  nodular 
or  purulent. 

The  purulent  form  of  peribronchitis  may  occur  as  an  inde- 
pendent affection,  characterized  by  a  purulent  infiltration  of 
the  smaller  and  ultimate  bronchial  tubes,  and  may,  for  a  long 
time,  be  unattended  by  lobular  consolidation.  Patients  in 
this  condition  may  have  many  of  the  rational  signs,  and  yet 
give  none  of  the  physical  signs  of  phthisis,  except  those  of 
localized  bronchitis.  After  a  time,  however,  the  neighbor- 
ing alveolar  parenchyma  necessarily  becomes  involved,  when 
the  evidences  of  lobular  consolidation  are  added  to  those  of 
localized  bronchitis. 

From  what  I  have  told  you  this  morning  concerning  the 
anatomical  changes  in  pulmonary  phthisis,  it  is  apparent 
that  peribronchitis  is  the  principal  and  most  important  pro- 
cess in  phthisical  developments.  It  may  also  be  regarded 
as  an  established  fact  that  tubercules  are  formed  in  the  lungs 
only  where  there  exists  connective  tissue,  lymphatics,  and 
very  fine  arteries  with  lymph  sheaths  ;  consequently,  they 
may  be  found  in  fibrous  layers  of  the  mucous  membrane  of 
the  large  bronchi,  in  the  walls  of  the  bronchioles,  in-  the  in- 
terlobular  connective  tissue,  and  in  the  walls  of  the  alveoli. 

15 


LECTURE    XIX. 


PULMONARY  PHTHISIS. 


Etiology  of  the  Different  Varieties. 

I  SHALL  this  morning  continue  the  history  of  pulmonary 
phthisis  by  inviting  your  attention  to  its  causation.  It  is 
not  until  quite  recently  that  this  part  of  its  history  has  to 
any  extent  engaged  the  attention  of  medical  observers. 
Although  we  may  not  be  able  to  cure  this  disease  when  once 
it  has  been  fully  developed,  yet,  with  our  present  knowledge 
of  its  etiology,  we  may  hope  to  be  able  to  prevent  its  devel- 
opment in  a  large  proportion  of  cases.  The  question  of  its 
causation  consequently  becomes  a  very  important  element 
in  its  history. 

ETIOLOGY. — In  order  to  systematize  our  knowledge  upon 
this  point,  I  shall  divide  the  causes  of  phthisis  into  general 
and  local. 

Under  the  head  of  general  causes,  I  shall  class, 

First. — Hereditary  or  acquired  feebleness  of  constitu- 
tion. 

Second. — Anti-hygienic  influences. 

Tliird. — Climate. 

Under  the  head  of  local  causes,  I  shall  consider : 

First.  — Bronchitis. 

Second. — Pneumonia  and  Pleurisy. 

Third.  — Mechanical  irritants. 

All  cases  of  pulmonary  phthisis  originate  in  obedience  to 
one  or  the  other  of  these  two  classes  of  causes,  or  to  both 
combined. 


PULMONARY   PHTHISIS.  227 

Let  us  first  inquire  in  regard  to  the  hereditary  causes  of 
phthisis. 

Hereditary  predisposition. — There  can  be  no  question 
but  that  certain  hereditary  influences  have  much  to  do  with 
predisposing  individuals  to  the  development  of  phthisis. 
It  has  been  maintained  by  some  careful  medical  observers 
that  phthisis  can  never  be  developed  in  a  person  who  has 
no  hereditary  tendency  to  the  disease.  Every-day  experi- 
ence disproves  such  a  sweeping  statement. 

On  the  other  hand,  equally  competent  observers  have 
maintained  that  phthisis  is  hereditary  only  in  comparatively 
few  cases.  This  statement  is  also  contrary  to  our  every-day 
experience. 

If  we  take  the  position  that  it  is  not  the  phthisis  that  is 
transmitted  from  parent  to  offspring,  but  a  feebleness  or 
vice  of  constitution  which  so  affects  the  individual  that  he 
is  liable  to  phthisical  developments  when  certain  local  causes 
are  brought  into  operation, — then,  hereditary  influences  as  a 
cause  of  phthisis  are  better  understood  and  more  fully  ap- 
preciated ;  especially  is  this  evident  when  it  can  be  shown 
that  this  vice  of  constitution  may  be  inherited  by  the  chil- 
dren of  the  aged,  of  drunkards,  of  those  enervated  by  ex- 
cesses of  any  kind,  or  of  those  who  at  the  time  of  the  birth 
of  their  children  were  suffering  from  some  form  of  constitu- 
tional disease,  such  as  cancer,  syphilis,  rheumatism,  etc.  I 
repeat,  when  it  can  be  shown  that  such  children  have  a 
hereditary  vice  of  constitution  which  allows  of  phthisical 
development,  equally  with  those  who  are  born  of  phthisical 
parents,  we  are  better  able  to  understand  the  exact  position 
which  the  question  of  hereditary  taint  occupies. 

It  is  therefore  necessary,  in  order  to  fully  appreciate  the 
predisposing  influences  of  hereditary  taint  in  any  given  case, 
to  know  exactly  the  condition  of  the  parents  at  the  time  of 
the  individual's  birth.  The  questions  to  determine  are: — 
Under  what  circumstances  was  he  born  ;  was  either  or  both 
of  the  parents  phthisical  at  the  time  of  his  birth  ;  were  they 
suffering  from  syphilis ;  were  they  intemperate ;  were  they 
old  and  feeble?  Under  any  of  these  circumstances,  or  cir- 
cumstances of  like  character,  there  has  been  transmitted  to 


228  ETIOLOGY. 

the  offspring  a  feebleness  of  constitution  which,  when  they 
are  subjected  to  certain  local  influences,  will  favor  phthisical 
developments. 

Anti-hygienic  Influences. — So  long  as  poverty  and  desti- 
tution shall  exist  on  the  one  hand,  and  dissipation  and  en- 
ervating luxury  on  the  other,  anti -hygienic  influences  must 
be  regarded  as  important  general  causes  of  pulmonary 
phthisis,  ranking  only  second  in  importance  to  hereditary 
influences. 

Impure  air,  improper  quality  and  insufficient  quantity  of 
readily  assimilated  food,  are  among  the  most  prolific  of  this 
class  of  causes. 

If  to  these  are  added  insufficient  clothing,  damp,  badly 
ventilated  apartments,  intemperance  in  the  use  of  alcoholic 
stimulants,  venereal  excesses,  prolonged  lactation,  repeated 
miscarriages,  want  of  cleanliness,  and  all  those  influences 
which  arrest  or  diminish  cutaneous  function,  we  have  a  most 
formidable  array  of  predisposing  causes. 

The  acquired,  feebleness  of  constitution  which  may  be  de- 
veloped by  a  combination  of  anti-hygienic  influences  in  early 
childhood,  as  well  as  in  adult  life,  is  unquestionably  as 
potent  a  cause  of  phthisis  as  hereditary  predisposition. 

It  needs  no  argument  to  prove  that  the  circumstances  un- 
der which  the  two  first  years  of  infantile  life  is  developed 
determine  to  a  great  extent  whether  the  foundation  for  a 
strong  and  vigorous,  or  for  a  weak  and  feeble  constitution  is 
being  laid. 

Let  a  healthy  child,  during  its  infancy  and  early  child- 
hood, be  subjected  to  the  influences  of  small,  badly  venti- 
lated apartments,  improper  diet,  and  all  the  other  attendant 
anti-hygienic  influences  of  the  tenement-house  population  of 
great  cities,  and  it  will  become  an  enfeebled  child,  so  that,  if 
it  reaches  the  years  of  maturity,  it  has  stamped  upon  it  a 
vice  of  constitution  which  is  ready,  upon  local  excitement, 
to  develop  pulmonary  phthisis.  Among  the  lower  classes, 
almost  the  entire  population  of  this  city  is  stamped  with  this 
influence  ;  and  whether  hereditary  tendency,  in  the  common 
acceptation  of  that  term,  is  or  is  not  present  in  this  class  of 
persons,  they  are  exceedingly  liable  to  the  development  of 


PULMONAEY  PHTHISIS.  229 

phthisis.  I  wish  to  lay  special  stress  upon  this  point,  for  I 
regard  it  as  one  of  the  most  important  in  the  whole  category 
of  general  causes. 

There  has  come  to  be  an  opinion  in  the  profession  that 
phthisis  is  certain  to  develop  sooner  or  later  in  those  who 
have  a  strong  hereditary  phthisical  predisposition  ;  that  be- 
cause the  father  or  mother,  or  brother  or  sister  has  died  of 
phthisis,  that  other  members  of  the  same  family  will  have 
the  disease ;  but  the  development  of  the  disease  in  every 
such  case  depends  more  upon  the  antecedent  hygienic  influ- 
ences under  which  the  childhood  or  adult  life  has  been 
passed,  than  upon  the  hereditary  phthisical  predisposition. 
These  predisposing  anti-hygienic  influences  embrace  the  im- 
portant problem  of  infantile  diet. 

How  few  infants  are  properly  fed  !  How  few  mothers, 
especially  among  the  wealthier  classes,  are  in  a  condition 
to  properly  nourish  their  own  offspring !  The  habit 
which  prevails  of  feeding  children  until  they  are  one, 
two,  or  even  three  years  of  age,  upon  barley  water,  paps, 
sweetmeats,  and  indigestible  articles  of  diet,  has  a  most 
pernicious  influence  upon  the  future  physical  development 
of  the  child,  and  if  at  the  very  entrance  upon  adult  life  of 
such  children,  phthisis  is  not  induced  by  some  local  cause, 
it  will  be  an  exception  to  the  rule.  Consequently,  in  mak- 
ing up  your  estimate  of  the  influences  which  may  foster  the 
development  of  phthisis  in  any  case,  it  is  important  first  to 
determine  the  condition  of  the  parents  at  the  time  of  the 
birth  of  the  individual,  then  the  hygienic  influences  under 
which  his  childhood  and  early  life  were  passed.  Because  a 
father  and  mother  have  died  of  phthisis,  it  is  not  neces- 
sarily developed  in  the  children.  It  becomes  one  of  the 
great  objects  of  physical  training  to  overcome  such  a  con- 
stitutional tendency,  and  it  can  be  accomplished  in  the 
majority  of  cases  before  the  age  of  puberty.  Good  hygienic 
surroundings,  and  systematic  physical  training  during  in- 
fantile and  early  life,  will  furnish  physical  power  sufficient 
to  resist  a  strong  hereditary  phthisical  tendency. 

If  phthisis  has  developed  in  one  member  of  a  family,  it  is 
all-important  that  the  children  of  that  family  should  be . 


230  ETIOLOGY. 

placed  under  such  hygienic  influences,  and  physical  training 
during  babyhood,  childhood,  and  early  manhood  or  woman- 
hood, as  shall  insure  the  greatest  amount  of  physical  yigor. 
A  mother  who  has  a  strong  phthisical  history,  hereditary  01 
acquired,  should  neyer  be  allowed  to  nurse  her  own  chil- 
dren ;  they  should  be  nursed  by  a  yigorous,  non-phthisi- 
cal wet-nurse. 

All  of  these  predisposing  phthisical  influences,  both  in 
childhood  and  adult  life,  meet  at  one  common  point,  and 
have  one  essential  method  of  operation,  viz.,  they  arrest 
physical  development,  and  thus  lessen  the  powers  of  resist- 
ance, placing  the  subject  in  a  position  where  he  is  readily 
acted  upon  by  the  local  causes  which  lead  to  the  develop- 
ment of  phthisis. 

Climate. — This  has  long  been  regarded  as  one  of  the  most 
powerful  causes  of  pulmonary  phthisis.  It  has  been  claimed 
that  climatic  influences  alone  are  sufficient  to  develop  phthi- 
sis, and  some  have  even  gone  so  far  as  to  take  the  position 
that  phthisis  is  not  developed  unless  the  individual  is 
placed  under  certain  climatic  influences. 

We,  however,  are  unacquainted  with  any  climatic  condi- 
tion which  renders  the  development  of  phthisis  a  necessity, 
or  that  makes  its  development  impossible  ;  still,  there  are 
climatic  conditions  which  are  antagonistic  to  its  develop- 
ment, as  well  as  those  which  favor  its  development.  With- 
out question,  the  disease  occurs  with  much  greater  frequency 
in  one  climate  than  in  another  ;  for  instance,  it  is  of  much 
more  frequent  occurrence  in  the  temperate  zone  than  in 
either  the  torrid  or  frigid.  It  is  a  question,  however,  if  cli- 
mate of  itself  can  properly  be  regarded  as  a  cause  of  phthisis  ; 
there  is  something  more  than  climatic  changes  in  those 
localities  which  are  especially  prolific  in  phthisical  develop- 
ments. 

There  can  be  no  question  but  that  altitude  is  a  mo<t 
powerful  climatic  element ;  as  a  rule,  phthisis  is  rarely  de- 
veloped in  a  moderately  high  altitude.  To  a  certain  rxtt-nt, 
the  climate  of  high  elevations  is  antagonistic  to  phthisical 
developments. 

Sudden  changes  of  temperature,  and  a  damp,  cold  atmos- 


PULMONARY   PHTHISIS.  231 

phere,  due  to  peculiar  conditions  of  the  soil  of  certain  local- 
ities, are  unquestionably  potent  causes  in  the  development 
of  phthisical  constitutions  ;  aside  from  these  conditions, 
climate  can  hardly  be  regarded  as  a  predisposing  cause  of 
phthisis.  The  locality  best  suited  to  any  phthisical  patient 
can  only  be  determined  by  trial ;  frequent  changes  unques- 
tionably are  important.  I  shall  consider  this  point  more 
fully  under  the  head  of  treatment. 

We  now  come  to  the  local  causes  of  phthisis  ;  these  are,  it 
seems  to  me,  more  powerful  than  the  general  causes. 

Under  this  head,  I  include  bronchitis,  pneumonia,  pleu- 
risy, and  mechanical  irritants. 

The  development  of  phthisis  from  attacks  of  bronchitis  is 
a  fact  long  known,  but  not  until  recently  fully  established. 
It  has  been  claimed  that  the  bronchitis  was  secondary,  and 
not  the  cause  of  phthisical  developments.  In  our  study  of 
the  morbid  anatomy  of  this  disease,  it  would  seem  that  you 
must  have  been  convinced  that  the  contrary  of  this  state- 
ment was  true,  and  that  bronchitis  gives  rise  to  a  large  pro- 
portion of  the  anatomical  changes  of  the  disease. 

Clinical  experience  establishes  the  fact  that  a  large  pro- 
portion of  cases  of  catarrhal  and  fibrous  phthisis  begin  with 
a  naso-pharyngeal  catarrh  which  gradually  extends  to  the 
larger  bronchi  and  then  to  the  bronchioles,  and,  as  has  al- 
ivady  been  shown,  finally  develops  lobular  pneumonia,  which 
1  c;tds  to  phthisical  developments.  Why  an  apparently  sim- 
ple catarrh  leads  to  the  development  of  phthisis  in  one 
case,  and  not  in  another,  can  be  readily  explained  by  refer- 
ence to  the  general  causes  of  the  disease  already  referred 
to.  When  an  individual  is  in  a  condition  to  resist  an  at- 
tack of  bronchitis,  usually  it  speedily  terminates  in  com- 
plete recovery  ;  but  if  any  or  all  of  the  predisposing  causes 
to  phthisical  develpment,  which  I  have  detailed,  are  in  op- 
eration, the  bronchial  catarrh  progresses  and  phthisis  is  the 
result. 

The  development  of  phthisis  from  pneumonia  has  already 
been  sufficiently  considered  in  connection  with  the  morbid 
anatomy  of  phthisis.  Pulmonary  phthisis  not  unfrequently 
dates  from  an  attack  of  subacute  pleurisy.  The  pleurisy 


232  ETIOLOGY. 

may  not  be  severe,  and  the  adhesions  between  the  two  sur- 
faces not  extensive,  but  the  lung  becomes  more  or  less  crip- 
pled in  its  action,  and  as  a  consequence  the  pulmonary  par- 
enchyma becomes  hypersemic,  and  catarrhal  processes  are 
established  which  terminate  in  cheesy  pneumonia,  or  some 
of  the  inflammatory  products  in  the  pleura  become  cheesy, 
and  form  a  nidus  for  the  development  of  miliary  granula- 
tion. Thus,  a  pleurisy  occurring  in  one  who  has  a  phthisical 
diathesis,  either  hereditary  or  acquired,  may  be  an  exciting 
cause  of  phthisis.  There  is  a  difference  of  opinion  in  the 
profession  as  to  the  power  of  bronchial  hemorrhage  to 
develop  phthisis.  Some  say  it  is  impossible,  while  others 
claim  that  it  is  not  of  infrequent  occurrence.  There  can  be 
no  question  but  that  a  bronchial  hemorrhage  is  frequently 
the  first  and  only  sign  of  phthisical  developments.  Those 
who  object  to  the  statement  that  hemorrhages  are  a  devel- 
oping cause  of  phthisis,  claim  that  there  is  something 
behind  the  hemorrhage.  Unquestionably,  a  bronchial  hem- 
orrhage indicates  a  vice  of  constitution  which  favors  phthi- 
sical developments,  but  it  requires  no  argument  to  prove 
that  it  does  not  afford  evidence  that  tubercles  exist  in  the 
lungs. 

The  connection  which  exists  between  phthisical  develop- 
ments and  bronchial  hemorrhage  is  by  no  means  clear  or 
satisfactory,  unless  the  blood  in  the  bronchi  be  regarded  as 
the  exciting  cause  of  the  bronchitis  which  follows  the  hem- 
orrhage and  leads  to  the  pneumonia  which  is  the  founda- 
tion of  the  future  phthisis. 

In  some  cases  the  rise  in  temperature,  and  other  pneumo- 
nic symptoms,  so  quickly  follow  the  occurrence  of  a  hemor- 
rhage in  lungs  that  prior  to  the  hemorrhage  gave  no  evi- 
dences of  disease,  as  to  leave  little  doubt  but  that  the  hem- 
orrhage preceded  if  it  did  not  excite  the  pneumonia. 

The  mec7ianical  irritation  of  the  bronchi  produced  by  the 
constant  inhalation  of  an  atmosphere  loaded  with  particles 
of  dust  or  grit  (as- occurs  in  certain  trades  and  occupations) 
often  leads  to  the  development  of  phthisis.  Although  there 
may  exist  no  hereditary  or  acquired  phthisical  diathesis, 
yet  when  constantly  inhaled  these  substances,  by  their  con- 


PL  IT  MOIST  ART   PHTHISIS.  233 

tinuous  mechanical  irritation,  excite  bronchial  inflammation  ; 
such  inflammation  is  not  limited  to  the  bronchial  mucons 
membrane  and  its  epithelium,  but  penetrates  deeper  and 
causes  destruction  of  the  parenchyma  of  the  lung.  When 
such  irritation  is  long-continued,  the  diseased  processes  grad- 
ually extend,  and  after  a  time  true  phthisis  is  developed. 

If  destruction  of  the  pulmonary  parenchyma  may  thus 
be  produced  in  a  non-phthisical  subject,  it  is  evident  that 
it  may  be  more  rapidly  and  extensively  developed  in  those 
having  strong  phthisical  tendencies. 

Such  admixtures  of  dust  and  air  as  are  present  in  work- 
shops and  large  manufactories  are  prolific  exciting  causes 
of  phthisis.  The  most  dangerous  occupations,  as  regards 
the  development  of  phthisis,  are  stone-cutting,  knife-grind- 
ing, steel-polishing,  diamond-cutting,  etc. 

The  constant  inhalation  of  noxious  gases,  such  as  are 
generated  in  over-crowded,  badly  ventilated  apartments,  is 
another  very  important  element  in  the  production  of  phthisis. 

The  etiology  of  tubercular  phthisis  is  still  undetermined. 
Recent  observations  seem  to  show  that  the  development  of 
tubercles  is  due  to  a  specific  infection,  and  that  the  neces- 
sary foundation  for  their  development  is  a  cheesy  mass,  and 
that  when  the  constituents  of  such  a  mass  are  taken  into  the 
blood  and  lymphatics,  a  multiple  development  of  tubercle  is 
produced.  It  is  claimed  that  the  localized  development  of 
tubercles  in  the  lungs  is  due  to  the  absorption  of  cheesy 
material  from  the  adjacent  tissues  through  the  lymphatics 
or  nutrient  canals.  This  process  is  generally  slow  ;  conse- 
quently, the  term  chronic  tuberculosis  has  been  applied  to 
this  form  of  tubercular  development. 

In  certain  instances  the  local  infection  is  followed  or  ac 
companied  by  a  general  infection,  which  is  due  to  the  intro 
duction  of  caseous  material  into  the  circulation,  and  tuber- 
cular developments  are  to  be  found  in  nearly  every  organ 
and  tissue  of  the  body. 

The  development  of  the  tubercular  granulations  under 
such  conditions  is  directly  due  to  the  absorption  of  the 
cheesy  material,  which  by  its  presence  in  the  blood  arouses 
a  formative  activity  in  the  connective-tissue  corpuscles  and 


234  SYMPTOMS. 

in  the  endothelium  of  the  lymphatics,  and  is  manifested  by 
the  production  and  proliferation  of  cells  and  nuclei. 

SYMPTOMS. — In  considering  the  symptoms  which  attend 
the  development  of  pulmonary  phthisis,  I  shall  first  speak 
briefly  of  those  which  are  especially  characteristic  of  tlu; 
different  varieties,  and  then  describe  in  detail  those  which 
are  common  to  all  varieties  of  the  disease. 

In  a  certain  class  of  cases  phthisis  commences  as  an 
acute  affection,  and  its  onset  is  marked  by  very  active 
symptoms  ;  this  is  the  case  when  acute  catarrhal  pneumonia 
passes  rapidly  into  caseous  infiltration.  Instead  of  the 
symptoms  of  resolution  coming  on  at  the  end  of  the  second 
or  beginning  of  the  third  week,  as  usually  is  the  case  in 
this  form  of  pneumonia,  the  temperature  of  the  patient 
rises  in  the  evening,  and  does  not  fall  in  the  morning, 
but  continues  higher  than  it  has  been  at  any  previous 
period  during  the  course  of  the  disease ;  soon,  a  regular 
morning  and  evening  variation  in  temperature  occurs,  ac- 
companied by  night-sweats,  which  stamp  it  as  hectic  in 
character  ;  this  is  accompanied  or  soon  followed  by  profuse 
expectoration,  which  contains  yellow  streaks,  in  which  may 
be  found  fatty  and  granular  epithelium,  with  fibres  of  elastic 
tissue,  and  occasionally  streaks  of  blood.  With  these 
sj^mptoms  there  is  a  rapid  loss  of  strength  and  flesh,  accom- 
panied by  the  other  general  symptoms  which  ordinarily  at- 
tend the  development  of  pulmonary  phthisis. 

Physical  examination  of  the  chest  will  determine  that 
pulmonary  consolidation  is  present,  and  following  close 
upon  this  will  be  the  physical  evidences  of  excavation,  and 
cavities  may  be  formed  in  the  lungs  of  such  patients  within 
two  or  three  months  after  the  commencement  of  their  ill- 
ness. Under  these  circumstances  the  diagnosis  of  acute 
pneumonic  phthisis  is  readily  made. 

The  form  of  phthisis  which  commences  as  a  tuberculosis 
differs  from  acute  pneumonic  phthisis  in  the  fact  that  the 
constitutional  symptoms  precede  the  manifestation  of  the 
local  symptoms. 

That  form  of  phthisis  which  immediately  follows  the  oc- 
currence of  a  profuse  haemoptysis  (which  some  believe  is 


PULMONARY   PHTHISIS.  235 

produced  by  the  effusion  and  coagulation  of  blood  in  the 
bronchi  and  air-cells)  usually  runs  a  rapid  course,  is 
pneumonic  in  its  character,  and  is  attended  in  its  develop- 
ment, after  the  occurrence  of  hemorrhage,  by  symptoms 
which  are  identical  with  those  which  attend  the  development 
of  acute  catarrhal  phthisis. 

When  an  individual  with  a  bronchial  catarrh,  which  com- 
menced as  a  "simple  cold — there  being  no  active  symptoms  to 
mark  its  advent  or  development,  with  scarcely  any  appreci- 
able disturbance  of  the  general  health — begins  to  lose  flesh 
and  strength,  grows  pale  and  thin,  the  cough  becoming 
paroxysmal  and  accompanied  by  a  tenacious  muco-purulent 
expectoration,  sometimes  streaked  with  blood,  there  is 
reason  to  suspect  that  the  alveoli  have  become  involved  in 
the  catarrhal  process,  and  that  cheesy  pneumonia  is  being 
developed ;  especially,  when  the  physical  signs  of  local 
consolidation  are  added  to  those  of  bronchial  catarrh. 
Under  such  circumstances,  we  have  developed  what  may  be 
termed  chronic  catarrhal  phthisis.  This  is  the  most  common 
variety  of  phthisis. 

Chronic  catarrhal  phthisis  may  also  occasionally  be  devel- 
oped from  an  acute  catarrhal  pneumonia.  When  this  oc- 
curs, the  acute  pneumonic  process  is  arrested  before  excava- 
tion occurs,  interstitial  pneumonia  is  developed,  the  fever 
subsides,  expectoration  diminishes,  the  patient  improves 
slowly,  but  never  fully  recovers,  and  more  or  less  extensive 
retraction  of  the  chest  takes  place  over  the  affected  portion. 

Fibrous  phthisis  is  distinguished  from  all  other  forms  of 
phthisis  by  its  greater  chronicity.  In  most  cases  it  com- 
mences as  a  chronic  affection,  coming  on  very  obscurely  ;  it 
is  characterized  by  the  local  signs  of  chronic  bronchitis  lim- 
ited to  one  lung.  In  some  cases,  cough  and  expectoration 
may  exist  for  a  long  period.  Sometimes  it  commences  as 
an  acute  affection,  either  as  an  acute  bronchitis  or  pneumo- 
nia ;  starting  in  this  manner  it  goes  on  in  much  the  same 
chronic  way  as  when  its  origin  is  obscure.  In  whatever 
manner  it  commences,  after  a  variable  length  of  time  the 
patient  commences  to  lose  flesh  and  strength  to  a  moderate 
extent,  cough  increases  and  expectoration  becomes  abun- 


236  SYMPTOMS. 

dant,  and  at  times  the  matter  expectorated  has  an  offensive 
odor ;  loss  of  appetite  ensues,  and  gradually  the  ordinary 
symptoms  of  pulmonary  phthisis  are  developed.  During 
all  the  time  which  has  been  occupied  in  the  development  of 
the  phthisical  symptoms  there  has  been  no  very  high  tem- 
perature or  very  rapid  pulse. 

Tubercular  phthisis  (as  I  have  already  stated)  differs  from 
the  other  varieties  in  the  fact  that  the  constitutional  symp- 
toms precede  the  local.  Usually,  for  some  time  prior  to 
the  development  of  local  symptoms,  the  patient  loses  flesh 
and  strength,  has  dyspeptic  symptoms  with  complete  loss 
of  appetite,  and  more  or  less  febrile  disturbance.  During 
this  period  he  continues  to  go  about,  but  constantly  com- 
plains of  physical  weakness  and  an  incapacity  to  do  any- 
thing which  requires  mental  application.  At  night  there  is 
more  or  less  profuse  sweatings,  and  the  patient  is  unable  to 
sleep  on  account  of  a  dry,  hacking  cough.  At  first,  these 
symptoms  are  attributed  to  dyspepsia  and  a  slight  attack  of 
bronchitis — there  is  nothing  about  the  case  to  lead  to  serious 
apprehension — a  careful  physical  examination  will  give 
negative  results.  Still,  the  cough  continues,  the  rise  in  tem- 
perature is  constant,  the  patient  is  unable  to  sleep  at  night, 
emaciation  goes  on  rapidly,  and  the  loss  of  flesh  is  accom- 
panied by  great  physical  weakness.  After  these  symptoms 
have  existed  two  or  three  weeks,  the  cough  begins  to  be 
accompanied  by  a  tenacious,  muco-purulent  expectoration, 
and  bronchial  rales  of  small  size  are  heard  over  the  entire 
chest,  leading  to  the  diagnosis  of  general  bronchitis.  The 
resonance  on  percussion  remains  normal,  the  respiration  now 
becomes  frequent,  short,  and  difficult,  and  the  patient  is  un- 
able to  lie  down  with  comfort.  In  five  or  six  weeks  from 
the  beginning  of  the  attack,  there  are  evidences  of  extensive 
pulmonary  consolidation,  and  the  patient  either  speedily 
manifests  the  symptoms  which  ordinarily  attend  the  stage 
of  softening  and  excavation  of  catarrhal  phthisis,  or  sinks 
into  a  stage  of  exhaustion  and  emaciation  analogous  to  that 
which  occurs  during  the  course  of  typhoid  fever.  In  either 
sase,  the  whole  progress  of  the  disease  is  marked  by  a  higher 
temperature  than  is  met  with  in  any  other  form  of  phthisis. 


PULMONARY  PHTHISIS.  237 

The  high  temperature  and  rapid  emaciation  at  the  nom- 
mencement  of  the  disease,  combined  with  absence  of  the 
local  signs  of  phthisical  process  in  the  lungs,  distinguish 
tubercular  from  the  other  varieties. 

I  shall  not,  at  this  time,  detail  to  you  the  distinguishing 
phenomena  which  attend  the  development  of  acute  general 
tuberculosis,  for  they  cannot,  strictly  speaking,  be  classed 
under  the  head  of  pulmonary  phthisis. 

The  thoracic  signs  and  symptoms  which  are  present  in 
acute  tuberculosis,  generally  are  secondary,  and  have  little 
to  do  with  the  destruction  of  life.  In  all  its  phenomena 
and  results  acute  tuberculosis  resembles,  and,  it  seems  to 
me,  should  be  classed  with  acute  blood  diseases.  It  is  the 
general  condition  of  the  patient,  and  not  any  local  pulmo 
nary  symptom,  which  characterizes  the  disease. 


LECTURE    XX. 


PULMONARY  PHTHISIS. 

Symptoms  Common  to  all  Varieties. 

1  SHALL  occupy  your  attention  this  morning  with  an 
analysis  of  those  symptoms  which  are  common  to  all  the 
varieties  of  pulmonary  phthisis.  The  symptomatology  of 
this  disease  cannot  be  divided  into  stages,  nor  does  the 
disease  pursue  any  regular  course ;  consequently,  I  shall 
consider  only  its  more  prominent  phenomena,  without  refer- 
ence to  the  order  of  their  occurrence.  I  shall,  as  far  as 
possible,  indicate  the  variety  of  the  disease  in  which  each 
prominent  symptom  is  most  likely  to  occur. 

I  will  first  speak  of  dyspnoea.  Increased  frequency  and 
difficulty  of  respiration  is  present  in  a  greater  or  less  degree 
in  all  varieties  of  phthisis  :  in  the  majority  of  instances  it  is 
marked  only  during  and  after  physical  exertion  ;  a  patient, 
even  in  the  advanced  stages  of  the  disease,  often  suffers 
very  little  from  dyspnoea  while  lying  quietly  in  bed ;  the 
respiration  may  be  somewhat  increased  in  frequency,  but 
ordinarily  it  is  not  laborious. 

When  dyspnoea  and  accelerated  breathing  occur,  their 
occurrence  is  due  to  a  variety  of  causes,— -first,  and  chiefly, 
to  fever  ;  second,  to  a  diminution  in  the  breathing  surface, 
consequent  upon  the  loss  of  lung-substance ;  third,  to  ob- 
structions in  the  bronchi ;  fourth,  to  pain  in  the  chest ;  in 
most  cases,  several  of  these  causes  are  combined.  The 
breathing-surface  of  the  lungs  may  be  greatly  reduced  in 
area  without  dyspnoea,  except  on  active  physical  exertion. 


PULMONAEY  PHTHISIS.  239 

Pain  and  obstruction  in  the  bronchi  always  give  rise  to 
more  or  less  difficulty  of  breathing,  especially  in  the  earlier 
stages  of  the  disease.  That  fever  causes  frequency  in  respi- 
ration is  evident,  and  the  reason  for  it  is  apparent.  The 
fever  of  phthisis  is  unquestionably  due  to  the  rapid  mole- 
cular metamorphosis  that  is  going  on  in  the  body ;  conse- 
quently there  is  an  extra  amount  of  carbonic  acid  formed, 
and  an  extra  amount  of  oxygen  required,  and  the  respira- 
tion must  necessarily  be  increased  to  supply  the  demand. 
When  fever  is  absent,  phthisical  patients  have  no  dyspnoea, 
except  so  far  as  it  may  depend  upon  a  diminished  amount 
of  breathing- surf  ace  and  pain  in  the  chest.  Under  such 
circumstances,  when  the  patient  is  quiet,  his  respiration 
may  be  almost  natural,  but  the  difficulty  will  immediately 
manifest  itself  on  exertion.  On  the  other  hand,  when  fever 
is  present,  especially  when  the  temperature  is  high,  there  will 
be  increased  frequency  of  respiration  at  all  times.  Frequency 
of  respiration  and  dyspnoea  may  also  to  some  extent  be  due 
to  the  accompanying  ansemia  and  cyanosis,  as  well  as  feeble- 
ness of  heart-action  from  fatty  degeneration  of  the  cardiac 
muscle. 

Pain  in  the  chest  is  not  a  very  prominent  or  constant 
symptom  of  phthisis  ;  it  is  never  present  to  any  very  great 
extent  except  in  connection  with  pleuritic  changes.  If  the 
pleura  is  not  involved,  usually  the  patient  will  be  com- 
paratively free  from  pain.  The  situation  of  the  pain  will 
correspond  to  the  situation  of  the  pleuritic  changes,  and  the 
character  of  the  pain  will  vary  with  the  activity  of  the 
pleuritic  processes.  Dry  pleurisies  often  occur  during  the 
progress  of  phthisis.  They  in  no  way  differ  in  their  anatom- 
ical changes  from  those  of  acute  pleurisy  already  described. 
They  always  depend  upon  morbid  changes  which  are  taking 
place  in  the  lung- tissue  beneath  the  pleura.  Such  pleuri- 
sies are  not  active,  and  are  attended  with  but  little  exuda- 
tion ;  they  cause  only  trifling  pain,  which  continues  for  a 
short  time  and  then  -passes  away,  to  return  again  after  a 
time ;  such  intermittent  attacks  may,  and  generally  do, 
continue  throughout  the  course  of  the  disease.  Sometimes 
phthisical  patients  suffer  more  or  less  pain  across  the  upper 


240  SYMPTOMS. 

portion  of  the  chest,  and  beneath  the  "shoulder-blade;" 
these  pains  are  also  pleuritic  in  character.  Pain  in  the 
chest,  during  the  progress  of  a  phthisis,  is  a  positive  symp- 
tom of  pleuritic  changes,  but  not  of  phthisis. 

Cough  is  one  of  the  earliest  and  most  constant  symptoms 
of  phthisis  ;  it  is  usually  present  at  the  very  onset  of  the 
disease,  and  continues  throughout  its  entire  course.  At 
first  it  is  dry,  paroxysmal,  or  hacking  in  character,  espe- 
cially in  the  earlier  stages.  It  may  exist  before  there  are 
any  appreciable  phthisical  developments,  and  then  ordi- 
narily it  is  accompanied  by  little  or  no  expectoration ;  if 
expectoration  does  occur,  it  is  small  in  amount,  tenacious 
in  character,  and  great  difficulty  attends  its  removal. 

Sometimes,  the  first  symptom  of  phthisis  will  be  violent 
paroxysmal  fits  of  coughing,  and  not  unfrequently  these 
paroxysms  will  be  so  violent  and  irritative  as  to  cause  the 
patient  to  vomit,  and  yet,  at  the  time,  physical  exami- 
nation will  furnish  no  evidence  of  lung-consolidation. 
Many  patients  cough  but  little  except  in  the  morning  after 
rising,  others  experience  several  paroxysms  during  the 
twenty-four  hours,  with  intervals  of  rest ;  while  sometimes, 
especially  in  advanced  phthisis,  there  are  no  such  intervals. 
Usually,  as  the  disease  progresses,  the  cough  becomes  more 
or  less  bronchial  in  character,  sometimes  has  a  rattling 
sound  ;  a  cough  which  is  bronchial  in  character  is  always 
accompanied  by  expectoration.  In  advanced  stages  of  the 
disease,  when  cavities  have  formed  in  the  lungs,  the  cough 
assumes  a  sepulchral  character. 

Expectoration. — At  first  this  may  be  composed  of  tena- 
cious mucus.  If  yellow  spots  are  found  in  the  mucus  ex- 
pectorated, you  may  be  certain  that  the  bronchial  catarrh 
has  reached  the  finer  bronchi ;  this  is  of  most  frequent  oc- 
currence in  catarrhal  phthisis.  If,  in  addition  to  these,  a 
little  further  on  in  the  progress  of  the  case,  streaks  of  blood, 
with  bronchial  and  alveolar  epithelium  in  a  state  of  fatty  or 
granular  degeneration,  are  found  in  the  expectoration,  it 
tells  you  of  chronic  broncho-pneumonia.  It  is  always  im- 
portant to  ascertain  whether  the  pallor,  fever,  and  emacia- 
tion of  your  patient  has  been  for  some  time  preceded  by 


PULMONARY  PHTHISIS.  241 

cough  and  expectoration,  or  whether  the  emaciation  pre- 
ceded the  cough  and  expectoration.  The  precursory  bron- 
chial catarrh  does  not  always  continue  the  same  length  of 
time  ;  it  may  reach  the  alveoli  as  early  as  the  second  week, 
or  it  may  exist  for  months  or  even  years,  until  at  some 
time,  when  the  individual  is  subjected  to  certain  depressing 
influences,  it  attacks  the  alveoli.  It  is  claimed  by  some 
that  in  a  certain  proportion  of  cases  desquamation  of  the 
alveolar  epithelium  precedes  the  bronchial  catarrh,  and  that 
the  catarrh  is  secondary  to  the  epithelial  desquamation ; 
clinical  observation,  however,  leads  us  to  bronchial  changes 
as  the  first  anatomical  changes  in  phthisical  developments. 

It  is  always  important  to  determine  the  exact  elements 
contained  in  the  sputa  ;  although  the  sputum  of  phthisis  is 
mainly  the  product  of  the  bronchial  catarrh  which  attends 
its  development,  still,  as  the  phthisical  processes  go  on, 
anatomical  elements  are  found  in  the  sputum  which  are 
diagnostic  of  the  disease.  Should  a  microscopical  ex- 
amination show  those  fine  yellow  streaks,  to  which  I  have 
already  referred,  to  contain  fatty  alveolar  epithelium  and 
shreds  of  elastic  tissue,  it  is  positive  evidence  that  a  phthi- 
sical process  has  been  established  in  the  lung,  although 
you  may  not  be  able  to  detect  it  by  physical  examination 
of  the  lungs.  Therefore  it  becomes  important  carefully  to 
examine  the  sputa  in  the  earlier  stages  of  the  disease  ;  you 
must  become  familiar  not  only  with  its  gross  appearance, 
but  with  its  microscopical  constituents. 

When  cavities  have  formed,  the  expectoration  changes. 
It  appears  in  rounded  masses  of  a  grayish  color  ;  these,  when 
thrown  into  a  cup,  will  remain  separated  from  each  other. 
When  these  masses  are  examined  microscopically,  they  are 
found  to  be  composed  of  young,  granular  cells,  showing 
evidences  of  fatty  metamorphosis,  entangled  with  small, 
annular  bodies  and  granular  detritus,  also  fibres  of  elastic 
tissue,  some  of  which  will  be  curved,  indicating  a  destruc- 
tive process  in  the  alveolar  walls.  Not  unfrequently,  small 
masses  of  cheesy  matter  are  found,  which  always  have  an 
offensive  odor.  These  lumps  of  cheesy  matter  may  be  of 
considerable  size.  Occasionally,  hardened  masses  of  calca- 

10 


242  SYMPTOMS. 

reous  matter  are  found,  indicating  that  an  old  process  has 
been  involved  in  the  excavation,  which  existed  prior  to  the 
present  phthisical  processes.  Blood-globules  arid  pus-glob- 
ules are  also  found  in  abundance.  If  there  is  any  doubt 
as  to  the  existence  of  a  cavity,  or  the  commencement  of  a 
softening  and  breaking-down  process,  the  expectoration 
should  always  be  subjected  to  a  careful  microscopic  exami- 
nation. 

The  quantity  of  the  expectoration  varies  very  much,  de- 
pending upon  the  extent  of  the  bronchial  catarrh,  and  the 
number  and  size  of  the  cavities. 

In  fibrous  phthisis  the  expectoration  will  vary  in  amount 
with  the  size  of  the  bronchial  dilatation.  When  there  is  lit- 
tle or  no  dilatation  of  the  bronchi,  the  expectoration  is  not 
very  abundant  and  is  tenacious  in  character;  but,  if  the 
bronchial  dilatation  is  extensive,  the  expectoration  is  abun- 
dant and  at  times  exceedingly  offensive. 

In  tubercular  phthisis  at  first  the  expectoration  is 
mucus,  but  as  the  case  progresses  it  does  not  differ  essen- 
tially from  that  of  catarrhal  phthisis.  When  either  variety 
has  reached  an  advanced  stage,  it  is  very  common  for  pa- 
tients in  the  morning  to  expectorate  a  thick,  yellow,  green- 
ish opaque  matter,  especially  after  a  quiet  night,  while 
during  the  remainder  of  the  day  it  is  yellow  and  less 
opaque. 

Fever. — Rise  in  temperature  is  the  most  constant  and 
important  symptom  of  pulmonary  phthisis,  and  is  due  to 
rapid  molecular  metamorphosis,  the  result  of  degenerative 
inflammatory  processes,  or  to  putrid  infections.  You  will 
rarely  meet  with  a  case  in  which  there  is  not  some  elevation 
of  temperature,  and  the  variations  which  occur  are  often 
very  great  and  follow  no  rule. 

In  catarrhal  phthisis,  the  invasion  of  the  alveoli  is  always 
marked  by  a  considerable  rise  in  temperature,  reaching 
often  102°  F.  or  103°  F. ;  if  it  continues  high  it  indicates  that 
the  pneumonic  process  is  extending,  and  more  lobules  are 
becoming  involved.  i 

In  fibrous  phthisis,  the  temperature  is  never  very  much 
elevated,  rarely  rising  above  100°  F.  ;  if  it  is,  the  elevation 


PULMOKAEY  PHTHISIS.  243 

is  an  accidental  one.  In  tubercular  phthisis,  the  tempera- 
ture is  high  from  the  very  commencement  of  the  disease, 
and  remains  high  throughout  its  whole  course,  ranging 
between  104°  F.  and  107°  F. ;  the  fever  is  continuous. 

If,  in  the  early  stage  of  phthisis,  the  fever  assumes  an  in- 
termitting type,  the  temperature  being  100°  F.  in  the 
morning,  and  102°  F.  in  the  evening,  you  may  be  almost 
certain  t;hat  you  have  to  do  with  a  catarrhal  form  of  phthi- 
sis ;  if,  on  the  other  hand,  the  fever  is  continuous  and  the 
temperature  ranges  high,  reaching  104°  or  105°,  you  may 
be  equally  certain  that  you  have  a  tubercular  phthisis. 

In  all  varieties  of  phthisis,  as  soon  as  softening  and  exca- 
vation occur  in  the  affected  portion  of  lung,  you  will  have 
developed  what  has  received  the  name  of  "  hectic  fever :" 
This  fever  usually  has  three  stages ;  a  cold  stage,  a  hot 
stage,  and  a  sweating  stage.  The  occurrence  of  the  three 
stages  is  not  necessary  to  establish  the  existence  of  the 
fever,  and  ordinarily  the  stages  do  not  follow  each  other 
with  any  regularity.  Sometimes,  in  the  course  of  the  day, 
the  patient  has  a  creeping,  chilly  sensation  which  may  last 
from  half  an  hour  to  an  hour, — then  there  will  be  felt  some 
dryness  and  heat  of  the  surface  ;  perhaps  the  temperature  in 
a  short  time  will  rise  to  103°  or  104°  ;  the  fever  lasts  a 
variable  length  of  time,  giving  to  the  face  that  peculiar 
brilliant  hue,  and  to  the  cheeks  that  peculiar  rosy  tint, 
which  is  so  characteristic  of  this  fever  ;  after  a  time  the 
fever  gradually  subsides,  and  sometime  in  the  course  of  the 
night  (it  may  be  near  morning)  comes  the  stage  of  sweating. 
These  night-sweats  are  usually  very  profuse,  and  when  so, 
are  very  exhausting.  Night-sweats  always  indicate  the 
existence  of  hectic  fever  and  constitute  a  part  of  it.  Chills 
or  rigors  are  often  wanting,  and  the  patient  may  be  igno- 
rant of  any  febrile  excitement,  but  the  night-sweats  are  a 
sure  indication  of  its  existence.  Another  leading  charac- 
teristic of  hectic  fever  is  its  irregularity  during  the  process 
of  excavation  ;  often  without  any  apparent  cause  it  disap- 
pears for  a  time.  Hectic  fever  may  occur  during  any  stage 
of  phthisis  ;  its  development  is  not  necessarily  due  to  soften- 
ing and  the  formation  of  cavities,  but  it  is  much  more  like- 


244  SYMPTOMS. 

ly  to  occur  then  ;  it  may  develop  at  the  very  commence- 
ment of  the  disease ;  when  it  occurs  early,  it  is  indicative 
of  tubercular  phthisis  or  extensive  purulent  peribronchitis. 

In  any  stage  of  phthisis,  as  soon  as  the  phthisical  process 
commences  to  retrograde,  the  retrogression  will  be  marked 
by  a  fall  in  temperature  ;  the  thermometrical  variation  will 
be  less,  the  morning  temperature  perhaps  normal,  and  the 
evening  temperature  only  a  degree  above  normal.  t  On  the 
other  hand,  any  new  accession  in  the  phthisical  develop- 
ments, or  extensive  septic  absorption,  will  be  indicated  by  a 
rise  in  temperature  by  at  least  one  or  two  degrees.  There- 
fore, in  every  case  of  phthisis,  daily  thermometrical  obser- 
vations are  of  importance,  for  they  positively  determine 
whether  the  case  is  progressing  favorably  or  unfavorably. 

Pulse. — The  pulse  is  almost  invariably  accelerated  in 
phthisis — for  the  most  part  it  corresponds  to  the  variations 
in  temperature ;  as  the  temperature  rises  there  will  be  a 
corresponding  acceleration  in  the  pulse. 

It  is  the  average  pulse  for  the  twenty-four  hours  that  is  to 
guide  you  in  your  observations,  for  there  is  no  disease  in 
which  there  is  such  a  rapid  rise  in  pulse  from  slight  exciting 
causes  as  in  phthisis ;  any  slight  excitant,  as  the  visit  of  a 
friend  or  physician,  will  cause  it  to  rise  twenty  beats  in  a 
few  moments.  In  the  early  stages  of  the  disease,  the  excita- 
bility of  the  pulse  is  often  its  most  striking  characteristic  ;  it 
is  always  feeble,  and  ranges  from  100  to  140  per  minute. 
An  improvement  in  the  other  symptoms  is  not  always  ac- 
companied by  an  improvement  in  the  pulse. 

In  tubercular  phthisis,  it  is  most  markedly  increased  in 
frequency ;  in  fibrous  phthisis  usually  it  is  nearly  normal, 
rarely  reaching  100  per  minute.  In  the  last  stage  of  ca- 
tarrhal  or  tubercular  phthisis,  the  pulse  becomes  very  rapid 
and  feeble. 

Emaciation. — This  is  a  very  constant  attendant  upon 
phthisical  developments,  but  it  is  not  always  a  progressive 
symptom,  especially  in  the  more  chronic  cases. 

Sometimes  emaciation  precedes  phthisical  developments, 
but  usually  when  this  occurs  the  emaciation  is  not  due  to 
phthisis. 


PULMONAEY   PHTHISIS.  245 

A  patient  commences  to  lose  flesh  and  strength ;  he  does 
not  cough  ;  his  principal  symptoms  are  those  of  dyspepsia  ; 
gradually  he  becomes  enfeebled  from  impaired  digestion 
and  nutrition ;  under  these  circumstances,  he  takes  cold  and 
has  a  slight  attack  of  bronchitis,  which  in  his  enfeebled  con- 
dition leads  to  phthisis  ;  the  loss  of  flesh  under  such  cir- 
cumstances is  not  necessarily  a  part  of  the  history  of  phthi- 
sis. When  phthisical  developments  precede  the  emaciation, 
or,  in  other  words,  the  other  signs  of  phthisis  exist  for  some 
time  before  the  individual  begins  to  lose  flesh,  fever  will  be 
the  principal  cause  of  the  emaciation,  on  account  of  the 
changes  in  nutrition  which  it  induces.  It  is  a  constantly 
high  temperature  which  indicates  the  most  rapid  molecular 
metamorphosis,  and  causes  the  most  rapid  emaciation. 

In  the  more  chronic  forms  of  catarrhal  phthisis,  and  in 
fibrous  phthisis,  the  emaciation  is  often  very  slow ;  patients 
with  these  forms  of  phthisis  are  constantly  losing  and  gain- 
ing flesh, -and  these  changes  may  continue  through  a  series  of 
years  ;  when,  however,  they  have  once  become  emaciated, 
they  seldom  regain  their  former  weight. 

In  tubercular  phthisis  the  emaciation  is  always  progres- 
sive and  rapid. 

With  the  emaciation  of  phthisis  there  is  associated  more 
or  less  anaemia,  and  a  consequent  change  in  the  color  of  the 
face  ;  it  assumes  a  peculiar  pearly  pallor,  which  is  quite 
characteristic,  and  when  the  hectic  fever  is  associated  with 
it,  the  face  may  assume  the  most  fascinating  flushes  of  ap- 
parent health. 

Loss  of  strength  also  attends  the  emaciation,  and  patients 
very  early  complain  of  great  debility  and  loss  of  muscular 
power. 

Digestion. — Disturbance  in  digestion  is  more  or  less  mark- 
ed in  almost  all  cases  of  phthisis.  As  a  rule,  the  desire  for 
food  is  diminished,  and  in  some  cases  there  is  entire  loss  of 
appetite,  and  even  repugnance  to  food.  The  opinion  that 
phthisis  has  its  primary  -seat  in  the  stomach  cannot  be  sus- 
tained ;  you  will  constantly  meet  with  cases  in  which  the 
digestive  powers  equal,  if  they  do  not  exceed,  those  of  per- 
sons in  health,  until  they  are  impaired  by  the  general  weak- 


246  SYMPTOMS. 

ness  which  results  from  the  progress  of  the  disease.  Vomit- 
ing, which  not  unfrequently  is  a  troublesome  attendant  upo» 
the  disease,  is  usually  reflex  in  character,  rather  than  de- 
pendent upon  a  diseased  condition  of  the  stomach,  and  the 
excessive  susceptibility  which  the  stomach  sometimes  mani- 
fests in  response  to  reflex  influences  renders  the  gastric 
symptoms  of  the  gravest  import. 

The  most  common  cause  which  acts  in  a  reflex  manner  to 
produce  vomiting,  is  the  violent  fits  of  coughing.  In  those 
cases  where  the  patient  complains  of  tenderness  and  heat 
in  the  epigastric  region,  and  vomits  bile  and  mucus,  the 
vomiting  is  due  to  the  presence  of  a  subacute  gastric  catarrh. 
It  is  important  in  treatment  to  distinguish  these  two  condi- 
tions. Usually  the  gastric  juice  is  sufficient  in  quantity, 
and  of  proper  quality,  to  readily  perform  stomach  digestion, 
if  the  food  can  be  retained  in  the  stomach  a  sufficient  length 
of  time. 

The  most  important  interference  with  digestion  which  oc- 
curs during  the  progress  of  phthisis  is  due  to  changes  which 
take  place  in  the  small  and  large  intestines.  These  intestinal 
changes  are  marked  by  the  occurrence  of  more  or  less  tym- 
panitis and  diarrhoea,  which  often  become  very  troublesome  ; 
few  altogether  escape  these  symptoms. 

DiarrJicea  in  phthisis  may  depend :  first,  upon  intestinal 
irritation  produced  by  undigested  food  ;  second,  upon  folli- 
cular  ulcerations  of  the  small  intestines — these  ulcerations 
are  rarely  tubercular  in  character  ;  third,  upon  ulcerations 
of  the  large  intestines.  The  diarrhoea  may  occur  at  any 
stage  of  phthisis,  but  it  is  more  likely  to  occur  in  the  latter 
stages,  and  unless  it  is  easily  controlled,  it  must  always  be 
regarded  as  an  unfavorable  symptom.  In  some  instances, 
diarrhoea  alternates  with  hectic  fever,  one  appearing  as  the 
other  subsides. 

Hcemoptysis  is  another  very  important  symptom  of  phthi- 
sis ;  it  may  occur  during  any  stage  of  the  disease,  and 
varies  in  quantity  from  a  slight  trace  of  blood  in  the  ex- 
pectoration to  a  pound  or  more.  Under  the  head  of 
bronchial  hemorrhage  and  pulmonary  apoplexy  I  have 
referred  to  the  different  sources  and  varieties  of  haemoptysis. 


PULMOISTAEY  PHTHISIS.  247 

Hemorrhages  that  occur  in  connection  with  the  develop- 
ment of  pulmonary  phthisis,  in  the  majority  of  instances 
are  bronchial,  and  the  blood  expectorated  is  arterial  in 
color.  When  streaks  of  blood  appear  in  the  sputa,  the 
bleeding  usually  comes  from  the  vessels  of  the  alveolar 
walls,  and  indicates  the  occurrence  of  lobular  consolidation. 
Profuse  hemorrhages  in  the  later  stages  of  phthisis  usually 
have  their  origin  in  cavities  of  the  lung- substance. 

The  hemorrhages  from  the  lungs  which  occur  in  the 
early  stages  of  phthisis  may  be  profuse,  but  they  are 
rarely,  if  ever,  immediately  fatal  or  dangerous  ;  but  profuse 
pulmonary  hemorrhages  in  advanced  phthisis  may  be  the 
direct  cause  of  death. 

Haemoptysis  usually  makes  its  appearance  with  coughing  ; 
it  is  to  be  distinguished  from  all  other  hemorrhages  from 
the  mouth,  by  the  arterial  red  color  of  the  blood,  which 
contains  more  or  less  air-bubbles,  giving  it  a  frothy  appear- 
ance, and  the  individual,  at  the  time  of  its  occurrence, 
experiences  a  sensation  as  if  some  fluid  was  trickling  be- 
neath the  sternum.  I  have  already  described  the  manner 
of  its  recognition  under  the  head  of  bronchial  hemorrhage. 
If  the  hemorrhage  is  very  profuse,  the  blood  will  sometimes 
rush  into  the  throat  and  excite  vomiting,  so  that,  at  first, 
you  will  regard  it  as  a  hsematemesis ;  as  the  hemorrhage 
subsides,  you  will  early  perceive  that  it  is  expectorated 
by  coug^i^g.  In  rare  cases,  when  the  bleeding  is  slight, 
the  blood  passes  into  the  mouth  without  exciting  any 
cough. 

We  now  come  to  the  question,  of  what  significance  is  the 
occurrence  of  haemoptysis  ?  Although  it  occurs  more  fre- 
quently in  connection  with  phthisical  developments  than 
with  any  other  pulmonary  disease,  and  there  are  compara- 
tively few  phthisical  subjects  who  do  not  have  one  or  more 
hemorrhages  ;  yet,  because  an  individual  has  had  a  hae- 
moptysis, it  is  by  no  means  certain  that  he  has  or  ever  will 
develop  phthisis. 

I  have  twice  had  the  opportunity  of  making  a  post-mor- 
tem examination  upon  a  person  who  had  had  several  attacks 
of  quite  profuse  haemoptysis  ;  in  both  cases  this  occurred  a 


248  SYMPTOMS. 

few  months  prior  to  death,  yet  I  found  the  lungs  free  from 
any  trace  of  disease. 

If  you  accept  the  views  already  stated  in  connection  with 
bronchial  hemorrhage,  you  readily  see  how  such  an  occur- 
rence is  possible.  In  a  large  proportion  of  cases  where 
haemoptysis  occurs  as  a  first  or  very  early  symptom  of 
phthisis,  it  simply  indicates  a  weakness  of  the  walls  of  the 
capillary  vessels  of  the  bronchial  membrane,  either  hereditary 
or  acquired,  which  favors  the  development  of  the  catarrhal 
process  which  leads  to  subsequent  phthisical  developments. 

You  may  always  allay  the  excitement  which  attends  the 
occurrence  of  a  hemorrhage  in  the  early  stage  of  phthisis, 
by  the  positive  statement  that  there  is  no  danger  or  cause 
for  alarm. 

Arrest  of  menstruation  is  of  very  frequent  occurrence 
in  the  course  of  phthisis  in  females,  and  generally  is  due 
to  the  attending  anaemia.  Its  occurrence  in  advancing 
phthisis  indicates  extensive  systemic  exhaustion,  and  is 
often  followed  by  a  more  rapid  progress  of  the  disease. 
Sometimes,  in  young  females,  suppression  of  menstruation 
is  one  of  the  very  first  prominent  symptoms  of  phthisis. 

Cerebral  symptoms  are  rarely  prominent  in  any  stage  of 
phthisis.  There  is  no  chronic  disease  in  which  the  mind  is 
clearer.  The  hopefulness  and  buoyancy  of  spirits  which 
attend  its  developments  are  truly  remarkable.  The  least 
improvement  in  the  symptoms  is  hailed  by  the  patient  as 
an  indication  of  commencing  recovery.  He  speaks  lightly 
of  his  unpleasant  symptoms,  a'nd  is  very  reluctant  to  admit 
that  his  disease  is  of  a  serious  nature, — rarely  will  a  phthis- 
ical patient  believe  that  recovery  is  not  possible. 

Changes  in  the  voice  are  due  to  the  laryngitis  wThich 
usually  accompanies  phthisical  development ;  the  laryngeal 
affection  is  often  very  slight,  but  it  is  seldom  entirely  absent. 

In  advanced  phthisis  it  often  gives  rise  to  the  most  dis- 
tressing symptoms,  such  as  permanent  loss  of  voice,  burning 
pain  in  the  larynx,  and  extreme  difficulty  in  deglutition. 
These  laryngeal  complications  are  always  unfavorable  symp- 
toms. 

I  have  already  discussed  the  character  and  significance  of 


PULM01STAEY   PHTHISIS.  249 

these  laryngeal  affections  under  the  head  of  chronic  laryn- 
gitis, and  therefore  shall  not  enter  into  detail  in  this  con- 
nection. 

(Edema  of  the  feet  and  legs  is  not  an  infrequent  symptom 
in  the  later  stages  of  phthisis,  and  the  gravity  of  this  symp- 
tom is  well  recognized  by  the  non-professional ;  its  occur- 
rence indicates  that  a  fatal  issue  is  not  far  distant.  This 
may  be  due  to  secondary  renal  changes,  but,  in  a  large  pro- 
portion of  cases,  it  is  due  to  thrombosis  of  the  veins  of  the 
lower  extremities,  which  takes  place  on  account  of  the  slow- 
ness of  the  return  circulation  from  enfeebled  heart-power ; 
the  thrombi  interfere  with  the  return  circulation,  and  oedema 
of  the  feet  is  the  result. 

Clubbing  of  the  terminal  phalanges  of  the  fingers  is  re- 
garded by  some  as  evidence  of  phthisis.  Unquestionably, 
it  is  frequently  met  with  in  connection  with  phthisical 
developments,  but  its  exact  relationship  to  phthisis  is  not 
determined. 

Some  ascribe  its  occurrence  to  interference  with  the  peri- 
pheral circulation  ;  others  regard  it  as  a  form  of  scleroderma, 
which  begins  in  the  finger-ends  and  extends  over  the  body, 
and  generally  ends  in  phthisis.  The  clubbing  doubtless  de- 
pends upon  hypertrophy  of  the  connective  tissue,  which  is 
analogous  to  pulmonary  cirrhosis. 


LECTURE  XXI. 


PULMONARY  PHTHISIS. 

Physical  Signs. — Differential  Diagnosis. 

I  SHALL  continue  the  history  of  the  symptoms  of  pulmo- 
nary phthisis,  by  inviting  your  attention  to  its  physical 
signs.  For  the  sake  of  convenience  in  describing  the  physical 
signs,  phthisis  has  been  divided  into  three  stages,  viz.:  a 
stage  of  consolidation,  a  stage  of  softening,  and  a  stage  of 
excavation.  It  is  very  difficult,  at  times,  to  draw  the  line 
of  distinction,  either  by  the  rational  symptoms  or  physical 
signs,  between  the  stage  of  softening  and  the  stage  of  exca- 
vation. I  shall,  however,  for  the  most  part,  retain  the  old 
division,  for  it  might  lead  to  confusion  if  only  two  stages 
were  recognized. 

In  the  first  stage  the  physical  signs  vary,  as  the  consoli- 
dation is  miliary  and  disseminated,  or  massive  and  involving 
large  portions  of  lung. 

It  must  be  borne  in  mind  that  phthisical  developments 
pre-eminently  involve  the  upper  portion  of  the  lungs  ;  the 
reason  for  this  has  already  been  given  in  the  description  of 
the  morbid  anatomy  of  the  disease. 

In  tlie  first  stage,  on  inspection,  expansion  on  inspiration 
in  the  infra  and  supra  clavicular  regions  of  the  affected  lung 
will  be  diminished.  In  some  cases  there  will  also  be  slight 
retraction  of  the  chest-walls  over  the  affected  portion  of 
lung,  but  this  retraction  will  not  occur  unless  the  consolida- 
tion is  quite  extensive,  and  the  disease  has  been  of  suffi- 


PULMONARY   PHTHISIS.  251 

ciently  long  standing  for  fibrous  induration  to  develop  in 
connection  with  the  other  phthisical  processes. 

Upon  palpation  the  loss  of  expansion  will  be  much  more 
distinctly  recognized  ;  indeed,  loss  of  expansion  can  be  de- 
tected by  palpation  when  it  is  not  apparent  by  inspection. 
As  a  rule,  vocal  fremitus  on  the  affected  side  will  be  slightly 
increased  ;  this  sign,  however,  is  of  but  little  importance  as 
a  diagnostic  element,  for  if  pleuritic  changes  have  occurred, 
vocal  fremitus  may  be  diminished  or  absent,  but  its  absence 
does  not  necessarily  indicate  that  consolidation  of  lung- 
tissue  is  not  present. 

Percussion.  —  The  percussion  sound  will  vary  with  the 
extent  of  the  consolidation,  and  the  condition  of  the  lung- 
tissue  surrounding  the  consolidated  portion.  If  the  consoli- 
dation is  slight  in  extent,  and  is  surrounded  by  either 
healthy  or  emphysematous  lung-tissue,  the  percussion  sound 
will  remain  normal.  Indeed,  when  localized  emphysema  of 
the  lung  surrounds  small  nodules  of  consolidation,  the 
resonance  on  percussion  over  the  consolidation  may  be  some- 
what exaggerated  ;  these  slight  changes  can  only  be  deter- 
mined by  a  comparison  of  the  two  sides.  Generally,  when 
the  existence  of  phthisical  consolidation  can  be  recognized 
by  percussion,  there  will  be  elevation  of  pitch  of  the  percus- 
sion sound  and  loss  of  pulmonary  resonance  over  the  affect- 
ed portion  of  lung.  At  first,  the  dulness  may  be  very  slight, 
but  it  will  become  more  and  more  marked  as  the  consolida- 
tion increases,  and  it  may  reach  complete  dulness  and  the 
disease  still  be  in  the  first  stage.  When  the  consolidation 
is  extensive,  marked  retraction  of  the  chest-walls  generally 
accompanies  it. 

When  practising  percussion,  if  you  would  recognize  a 
slight  consolidation  at  the  apex  of  the  lung,  it  is  important 
to  percuss  from  the  trachea,  rather  than  toward  it.  This 
precaution  is  important  for  the  reason  that  slight  consolida- 
tion will  pass  unrecognized,  if  there  is  a  large  amount  of  air 
in  its  immediate  neighborhood,  such  as  always  exists  in  the 
trachea.  In  accordance  with  the  same  principle,  there  is  a 
slight  difference  in  the  percussion  sound  over  healthy  lung 
at  the  end  of  a  full  inspiration  and  a  full  expiration  ;  when 


Olr  M-A1 

I-  K  \  s  I  C  (  A  K  b 


252  PHYSICAL   SIGXS. 

consolidation  exists,  there  will  be  no  such  difference.  In 
any  case,  if  doubts  arise  as  to  the  existence  of  a  slight 
consolidation,  percussion  should  be  performed  at  the  end 
of  a  full  inspiration,  and  also  at  the  end  of  a  full  ex- 
piration. 

Auscultation. — In  the  first  stage  of  phthisis,  the  results 
of  auscultation  vary  greatly  in  different  cases.  You  may 
find  the  respiratory  sounds  feeble,  or  almost  entirely  absent 
at  some  points,  and  exaggerated  at  others, — the  respiration 
may  be  interrupted  or  cog-wheeled  in  its  rhythm,  these 
changes  being  localized  at  the  point  where  you  have  recog- 
nized loss  of  expansive  movement  in  the  chest-walls  and 
detected  dulness  on  percussion. 

Again,  the  respiratory  murmur  may  be  changed  in  its 
quality.  It  may  be  rude  or  bronchial, — it  may  be  rude  and 
wavy,  or  rude  and  interrupted-, — it  also  may  be  feeble  and 
still  rude,  and  not  unfrequently  you  will  meet  with  exag- 
gerated rude  respiration. 

The  bronchial  element  in  the  respiratory  sound  will  cor- 
respond to  the  amount  of  pulmonary  consolidation.  When 
the  consolidation  is  only  slight,  there  will  be  only  a  slight 
rise  in  pitch, — the  respiratory  sound  will  lose  its  soft 
breezy  character  and  be  exaggerated,  feeble,  or  wavy.  Pro- 
longed expiration  has  no  significance  in  connection  with 
phthisis,  unless  it  is  of  high  pitch.  When  the  respiration 
is  rude  in  character,  and  the  inspiratory  sound  is  high- 
pitched,  there  is  a  distinct  interval  between  inspiration  and 
expiration,  and  the  expiratory  sound  is  prolonged  and 
higher  pitched  than  the  inspiration.  It  is  the  element  of 
high  pitch  that  distinguishes  the  prolonged  expiration  of 
phthisis  from  the  prolonged  expiration  of  emphysema. 
Over  the  portion  of  lung  not  involved  in  the  phthisical  pro- 
cess, the  respiration  will  be  exaggerated,  which  is  simply 
an  evidence  of  the  increased  amount  of.  labor  which  the 
healthy  lung-substance  is  called  upon  to  perform. 

Accompanying  and  often  preceding  the  changes  which  take 
place  in  the  respiratory  sounds,  there  will  be  heard  rales, 
which  vary  greatly  in  size  and  in  character.  These  rales 
may  be  mucous  rales  of  large  and  small  size,  subcrepitant 

UJOG 


PULMONARY   PHTHISIS.  253 

rales,  and  occasionally  crepitant  rales ;  the  small  mucous 
and  subcrepitant  rales  are  the  most  frequent,  and  these  are 
most  distinctly  audible  after  coughing.  If  the  consolida- 
tion is  extensive,  these  rales  will  assume  a  sharp  metallic 
quality.  Generally,  there  is  associated  with  these  rales 
high-pitched  crackling  sounds,  which  depend  on  changes 
that  have  taken  place  in  the  pleura  ;  these  pleuritic  sounds 
are  the  result  of  the  dry  pleurisies  which  always  accompany 
the  other  phthisical  processes  that  are  going  on  in  the  lung- 
substance.  It  has  been  claimed  by  some  that  all  the  rales 
which  are  heard  in  this  stage  of  phthisis  are  produced  upon 
the  surface  of  the  lung,  and  not  in  its  substance.  This  cer- 
tainly is  a  sweeping  statement,  too  much  so  to  be  exact,  for 
these  sounds  are  usually  circumscribed, — they  can  be 
changed  by  coughing  and  not  unf  requently  entirely  removed 
by  violent  coughing,  and  they  are  often  audible  before  the 
inspiration  is  completed.  If  they  were  friction-sounds, 
they  would  remain  after  coughing,  and  would  not  be 
changed  in  size,  character,  or  position.  These  sounds  also 
vary  very  much  at  different  examinations,  which  would  not 
be  the  case  if  they  were  pleuritic.  Unquestionably,  pleu- 
ritic friction-sounds  are  of  quite  frequent  occurrence  in 
connection  with  phthisical  developments ;  but  that  they 
afford  an  explanation  of  the  rales  that  are  heard  over  por- 
tions of  lung  that  are  the  seat  of  phthisical  changes,  can 
hardly  be  credited ;  in  fact,  carefully-conducted  post-mor- 
tem examinations  show  that  the  pleuritic  changes  in  the 
majority  of  instances  are  secondary  rather  than  primary  to 
the  phthisical  changes  in  the  lung-substance. 

Vocal  resonance  may  or  may  not  be  increased  ;  when  the 
consolidation  is  slight,  it  is  usually  only  slightly  increased  ; 
when  the  consolidation  is  extensive,  the  resonance  may  be 
very  much  intensified,  amounting  to  bronchophony.  If  the 
pleura  is  very  much  thickened  over  the  consolidated  por- 
tion, the  vocal  sound  may  be  feeble.  The  vocal  sounds  are 
subject  to  so  great  variations,  that  they  are  valueless  as 
a  basis  of  diagnosis.  Slight  exaggerated  vocal  resonance 
at  the  right  apex  of  the  lung  can  hardly  be  regarded  as  an 
evidence  of  phthisis ;  at  the  left  apex,  it  is  of  more  impor- 


254  PHYSICAL   SIGNS. 

tance.  We  now  come  to  the  physical  signs  which  are  indi- 
cative of  the  second  stage  of  phthisis. 

Second  stage. — In  this  stage,  as  ordinarily  regarded,  you 
will  find  that  all  the  physical  signs  which  have  been  de- 
scribed as  existing  in  the  first  stage  have  become  more 
marked,  and  new  auscnltatory  signs  referable  to  the  stage 
of  softening  are  developed. 

Inspection  shows  greater  frequency  in  the  respiratory 
acts,  and  a  more  marked  depression  above  and  below  the 
clavicle  on  the  affected  side,  as  well  as  an  increased  deficien- 
cy in  local  expansion,  especially  during  a  forced  inspiration. 

Percussion  elicits  a  more  widely  spread  and  a  more  intense 
dulness,  which  often  assumes  a  wooden  or  tubular  character. 

Auscultation  gives  a  more  intense  bronchial  respiration, 
and  more  abundant  moist  sounds  of  a  crackling  character. 
You  will  mark  the  appearance  of  softening,  not  so  much  by 
any  change  in  the  character  of  the  respiration,  or  marked  al- 
teration in  the  percussion  sound,  as  by  the  occurrence  of  cir- 
cumscribed localized  rales,  more  or  less  abundant,  bubbling 
and  oftentimes  sharp  and  crackling  in  character.  Already 
you  may  have  recognized  the  existence  of  mucous  rales, 
but  now  you  will  detect  at  certain  points  a  number  of 
moist  crackling  bubbles,  which  are  constant ;  they  remain 
unaffected  by  coughing,  and  will  be  found  unchanged  at 
successive  examinations.  Such  developments  are  strong  in- 
dications that  softening  has  commenced.  If,  in  addition, 
there  is  considerable  elevation  in  temperature,  and  fibres  of 
yellow  elastic  tissue  are  present  in  the  expectoration,  the 
existence  of  pulmonary  softening  is  established  beyond  a 
reasonable  doubt. 

It  is  always  important  to  determine  whether  softening  has 
or  has  not  taken  place,  and  it  is  frequently  a  very  difficult 
point  to  settle  ;  but  the  careful  study  of  a  case  in  the  man- 
ner already  indicated  will  rarely  fail  to  lead  you  to  a  correct 
conclusion. 

Third  stage. — In  this  stage  the  physical  signs  will  vary 
as  in  the  other  stages,  according  to  the  different  conditions 
of  the  lung,  and  very  marked  variations  in  the  physical 
signs  will  be  noticed  at  different  examinations,  made  within 


PULMONAEY  PHTHISIS.  255 

a  few  hours  of  each  other.  The  principal  physical  signs  of 
this  stage  are  produced  by  the  presence  of  cavities  in  the 
lung- substance,  and  the  diagnosis  of  cavities  depends  upon 
their  nearness  to  the  surface  of  the  lung,  their  size,  and  the 
condition  of  the  surrounding  lung-substance.  A  cavity,  to 
•be  recognized  with  certainty,  must  be  larger  than  a  hazel- 
nut,  near  the  surface  of  the  lung,  and,  for  the  most  part, 
contain  air,  and  have  a  free  communication  with  a  bronchial 
tube.  In  this  stage  inspection  and  palpation  will  show  a 
greater  depression  in  the  clavicular  and  infra-clavicular  re- 
gion than  in  either  of  the  preceding  stages,  and  there  is 
more  complete  absence  of  expansive  movements  during  the 
respiratory  acts. 

The  percussion  sound  will  vary  very  much  according  to 
the  condition  and  size  of  the  cavities,  and  their  surround- 
ings. If  a  layer  of  healthy  lung-tissue  intervene,  between 
the  chest-wall  and  the  cavity,  gentle  percussion  will  give 
normal  resonance,  while  forcible  percussion  (if  the  cavity 
is  filled)  will  elicit  deep-seated  dulness.  If  the  cavity  is 
empty,  the  percussion  sound  will  be  exaggerated,  and  per- 
cussion will  fail  to  detect  its  existence. 

When,  however,  a  cavity  which  is  of  large  size  and 
empty,  communicates  freely  with  a  bronchial  tube,  and  is 
situated  near  the  surface  of  the  lung,  or  surrounded  by 
consolidated  lung-tissue,  percussion  will  give  an  amphoric 
or  cracked-pot  resonance,  which  may  exist  even  when  the 
cavity  is  partially  filled  with  fluid.  Such  resonance  is 
obtained  in  the  following  manner :  direct  the  patient  to 
open  his  mouth,  then  make  forcible  percussion  immediately 
over  the  cavity,  and  the  forcible  expulsion  of  air  from  the 
cavity  produces  the  chink,  or  cracked-pot  resonance ;  if, 
however,  such  a  cavity  is  filled  with  fluid,  complete  dulness 
will  be  obtained,  when,  perhaps  only  a  few  hours  previous, 
amphoric  or  cracked-pot  resonance  was  present ;  when  the 
cavity  is  again  emptied,  the  resonance  will  return.  Occa- 
sionally, cracked-pot  resonance  will  disappear,  and  remain 
absent  for  some  time,  and  no  evidence  of  a  cavity  can  be 
found  where  one  was  known  to  have  previously  existed. 
This  happens  when  the  bronchial  tube  which  has  com- 


256  PHYSICAL   SIGHTS. 

municated  with  the  cavity,  becomes  obstnicted  in  such  a 
manner  as  to  prevent  the  ingress  of  air  and  the  egress 
of  fluid.  Generally  there  is  an  elevation  of  temperature 
when  this  occurs ;  after  a  time,  a  violent  paroxysm  of 
coughing  may  be  accompanied  and  followed  by  a  profuse 
expectoration,  then  it  is  said  that  an  "abscess  has  broken 
in  the  lungs, ' '  and  amphoric  resonance  may  again  be  estab- 
lished. 

The  auscultatory  signs  in  this  stage  of  phthisis  will  also 
vary  according  to  the  size  and  condition  of  the  cavity  ;  over 
a  cavity  of  small  size,  having  walls  which  will  yield  on 
inspiration,  and  collapse  on  expiration,  cavernous  respira- 
tion will  be  heard  ;  this  is  recognized  by  its  soft  blowing  cha- 
racter. It  has  no  vesicular  element,  is  lower  in  pitch  than 
bronchial  respiration,  and  has  a  peculiar  puffing  quality. 
Cavernous  respiration  is  more  likely  to  be  developed  in 
acute  than  in  chronic  phthisis,  in  cases  where  the  cavity  has 
been  developed  rapidly,  and  consequently  liable  to  have 
soft,  yielding  walls.  When  the  cavity  has  been  developed 
slowly,  and  is  surrounded  by  firm,  tense  walls,  amphoric 
respiration  will  be  heard.  The  presence  of  amphoric  respi- 
ration indicates  that  a  cavity  of  considerable  size  has  devel- 
oped in  consolidated  lung-tissue,  and  that  its  walls  are  firm 
and  tense,  and  do  not  yield  on  inspiration,  or  collapse  on 
expiration  ;  the  amphoric  quality  is  sometimes  most  marked 
with  inspiration,  and  again  with  expiration ;  it  has  a  peculiar 
metallic  quality  that  distinguishes  it  from  all  other  respi- 
ratory sounds.  When  cavities  are  partially  filled  with 
fluid,  so  that  the  fluid  shall  rise  to  the  level  of  the  bronchial 
opening  into  the  cavity,  the  air,  as  it  passes  into  the  cavity 
from  the  bronchial  tube,  will  agitate  the  fluid  in  the  cavity, 
causing  bubbles  to  burst  upon  its  surface,  giving  rise  to 
sounds  which  are  called  gurgles.  Gurgles  have  a  metallic 
quality,  which  distinguishes  them  from  mucous  rales  ;  they 
are  more  abundant  and  distinct  after  and  during  coughing. 
Gurgles  vary  in  size  and  character  according  to  the  size  of 
the  cavity  and  the  quality  of  the  fluid  present  in  the  cavity  ; 
the  thinner  the  fluid,  the  more  bubbling  the  sound.  When 
the  fluid  is  thick,  the  gurgles  are  more  crackling  in  charac- 


PULMONARY    PHTHISIS.  257 

ter,  and   closely  resemble  pleuritic   cracklings,    but  their 
metallic  quality  determines  their  origin. 

When  cavities  are  of  large  size  and  contain  thin  liquid, 
metallic  tinkling  sounds  may  be  produced  during  coughing, 
and  by  the  voice. 

The  vocal  sounds  over  large  cavities  have  a  metallic  or 
musical  quality.  I  regard  the  presence  of  the  amphoric  or 
cavernous  whisper  as  one  of  the  most  positive  physical  evi- 
dences of  pulmonary  excavation. 

Murmurs  in  the  subclavian  artery  are  not  unfrequently 
heard  during  the  different  stages  of  phthisis ;  the  exact 
anatomical  changes  which  give  rise  to  these  murmurs  has 
not  been  determined ;  pleuritic  thickenings  and  adhesions  at 
the  apex  of  the  lungs  have  been  regarded  by  some  as  the 
cause  of  their  occurrence  :  it  is  certain  that  these  murmurs 
are  more  frequently  met  with  in  phthisical  subjects  than  in 
the  healthy. 

The  respiration  in  the  unaffected  portions  of  lung  is  exag- 
gerated, and  the  percussion  sound  extra-resonant. 
•  DIFFERENTIAL  DIAGNOSIS. — The  differential  diagnosis  of 
pulmonary  phthisis  necessitates  a  comparison  between  it 
and  almost  every  other  form  of  pulmonary  disease. 

Bronchitis,  pleurisy,  pneumonia,  pulmonary  apoplexy, 
and  bronchial  hemorrhage  are  all  liable  to  be  confounded 
with  phthisis,  and  it  is  not  unfrequently  a  very  difficult 
task  to  draw  the  line  of  distinction  between  these  diseases 
and  phthisis. 

In  considering  this  question,  I  shall  start  with  this  state- 
ment, that  consolidation  of  lung-tissue  is  one  of  the  essen- 
tials in  the  diagnosis  of  phthisis. 

First,  let  us  consider  the  points  of  differential  diagnosis 
between  bronchitis  and  phthisis.  In  many  cases,  it  is  not 
only  important,  but  often  very  difficult  to  do  this,  for,  as 
I  have  already  stated,  in  a  large  proportion  of  cases  of 
phthisis,  bronchial  catarrh  is  the  starting-point  of  phthisi- 
cal development.  So  long  as  a  bronchitis  is  accompanied 
by  only  a  moderate  febrile  movement,  the  temperature 
ranging  below  100°  F.,  and  the  physical  signs  showing  that 
the  bronchitis  is  general,  phthisical  developments  are 
17 


258  DIFFERENTIAL  DIAGNOSIS. 

readily  excluded,  but  if,  in  the  course  of  a  bronchial  catarrh, 
the  temperature  rises  to  102°  F.  or  103°  F. ,  and  this  elevation  is 
accompanied  by  the  development,  at  the  apex  of  either  lung, 
of  localized  subcrepitant  rales,  which  are  persistent,  also, 
by  localized  dulness  on  percussion  over  the  seat  of  the  rales, 
and  a  bronchial  character  to  the  respiratory  murmur,  you 
have  reason  to  believe  catarrhal  phthisis  is  being  developed. 
If,  with  these  symptoms,  there  is  a  gradual  loss  of  flesh  and 
strength,  the  cough  becoming  hacking  in  character,  and  if  the 
expectoration  contains  fine  yellow  streaks,  with  blood-stains 
and  fatty  and  granular  epithelium,  you  may  be  almost 
certain  that  phthisical  developments  are  taking  place. 

The  differential  diagnosis  between  chronic  bronchitis  and 
fibrous  phthisis  rests  almost  entirely  upon  the  physical 
evidences  of  pulmonary  consolidation  and  retraction  in 
phthisis,  and  the  absence  of  these  in  simple  bronchitis. 

Acute  tubercular  phthisis  cannot  be  distinguished  from 
general  capillary  bronchitis,  except  by  the  high  temperature 
and  rapid  emaciation  which  accompany  the  phthisis.  In 
both  you  have  only  the  physical  signs  of  bronchitis  ;  if  hae- 
moptysis occur,  you  may  consider  tubercular  phthisis  to  exist. 

The  symptoms  that  attend  typhoid  fever,  complicated  by  a 
catarrhal  or  croupous  pneumonia,  so  closely  resemble  those 
of  acute  miliary  tuberculosis  that  the  differential  diagnosis 
is  always  difficult  and  often  impossible ;  the  most  efficient 
aid  in  establishing  the  diagnosis  under  these  circumstances 
is  a  microscopic  examination  of  the  sputa.  By  a  careful 
microscopic  examination  of  the  sputa  you  will  be  able  to 
diagnose  riot  only  acute  miliary  tuberculosis,  but  dissemi- 
nated cheesy  pneumonia  at  the  very  commencement  of  the 
attack.  It  is  also  often  very  difficult  to  distinguish  puru- 
lent peribronchitis  from  localized  tubercular  phthisis,  for 
there  is  nothing  distinctive  either  in  the  sputa  or  in  the 
physical  signs  ;  the  differential  diagnosis  can  only  be  made 
by  the  progressive  history  of  the  case. 

Croupous  pneumonia  involving  the  apex  of  a  lung  will 
give  rise  to  all  the  physical  signs  of  the  first  stage  of  phthisis. 
Under  such  circumstances,  the  differential  diagnosis  can 
only  be  made  by  taking  into  account  the  history  of  tb« 


PULMONAEY   PHTHISIS. 

case.  If  you  can  determine  that  the  signs  of  consolidation 
have  existed  for  several  weeks  with  little  or  no  change, — 
that  the  temperature,  at  no  time,  has  been  below  100°  F.,— 
that  the  patient  steadily  has  been  losing  flesh  and  strength, 
— has  had  night-sweats  and  an  abundant  purulent  expecto- 
ration, you  have  reason  to  believe  that  the  case  is  one  of 
phthisis  ;  although  the  disease  may  have  commenced  as  an 
acute  pneumonia,  the  pneumonia,  instead  of  passing  on  to 
resolution,  is  becoming  cheesy,  which  may  be  regarded  as 
the  first  stage  of  phthisis. 

The  diagnosis  between  pleurisy  and  phthisis  is  usually 
readily  made.  The  question  of  greatest  difficulty  to  decide 
is,  _Can  the  two  diseases  exist  at  the  same  time  in  the  same 
individual  ?  In  pleurisy  with  serous  effusion,  exaggerated 
respiration  is  usually  developed  in  the  upper  portion  of  the 
affected  side  ;  if,  however,  the  pressure  of  the  fluid  is  suffi- 
cient to  cause  compression  of  the  lung,  the  respiration  will 
become  bronchial  in  character,  and  as  a  sequence  broncho- 
vesicular  respiration  may  remain  after  the  fluid  has  disap- 
peared,—the  patient  being  feeble,  with  a  hacking  cough  and 
shortness  of  breath,  a  question  arises  as  to  the  existence  of 
phthisis  which  is  not  always  readily  answered.  Careful 
thermometrical  observations  alone  will  enable  you  to  settle 
the  question.  If  phthisical  developments  are  taking  place, 
the  temperature  will  range  from  100°  F.  to  103°  F.  ;  if  they 
are  not,  the  temperature  will  range  below  100°  F. 

A  localized  (also  called  dry)  pleurisy  occurring  at  the 
apex  of  a  lung,  which  has  not  been  preceded  by  a  general 
pleurisy,  usually  indicates  changes  in  the  lung'  which  are 
phthisical  in  their  nature  ;  when  these  changes  are  present, 
the  physical  signs  of  the  pleurisy  obscure  those  of  the  pul- 
monary changes. 

The  diagnosis  between  phthisis  and  pulmonary  infarction 
occurring  in  connection  with  pulmonary  hemorrhages,  rests 
altogether  upon  the  existence  or  non-existence  of  cardiac 
disease;  if  haemoptysis  occur,  with  localized  pulmonary 
consolidation  in  connection  with  heart  disease,  especially 
if  the  blood  expectorated  is  of  a  dark  color,  you  may  be 
almost  certain  that  it  is  not  of  phthisical  origin. 


260  DIFFERENTIAL   DIAGNOSIS. 

When  cavities  exist  in  the  lungs,  the  question  of  differ- 
ential diagnosis  is  never  difficult  if  you  correctly  appreciate 
the  physical  signs,  and  make  a  careful  examination  of  the 
sputa.  Previous  to  the  formation  of  cavities  it  may  some- 
times, as  I  have  shown,  be  difficult  to  recognize  the  existence 
of  phthisis  ;  but  all  doubts  disappear  as  soon  as  excavation 
takes  place.  I  will  briefly  recapitulate  the  diagnostic 
evidences  of  the  first  stage  of  phthisis  : 

A  dry,  hacking  cough,  with  gelatinous  expectoration, 
containing  bronchial  and  alveolar  epithelium  in  a  state  of 
fatty  metamorphosis,  sometimes  streaked  with  blood,  hae- 
moptysis, emaciation,  gradual  loss  of  strength,  increasing 
pallor,  dyspnoea  on  exertion,  flying  pains  about  the  chest, 
pulse  and  temperature  steadily  ranging  above  100°  F.,  loss 
of  appetite,  and  dyspeptic  symptoms.  If,  in  connection  with 
these  symptoms,  you  find  under  one  clavicle  dulness,  how- 
ever slight,  on  percussion,  accompanied  by  a  feeble  inspi- 
ratory  murmur,  or  if  the  inspiration  be  rude,  jerking,  or 
cogged-wheel  in  character,  and  the  expiration  is  prolonged 
and  high-pitched,  and  if  on  deep  inspiration,  or  after 
coughing,  a  few  clicks  or  dry  crackling  rales  are  heard,  you 
are  warranted  in  making  the  diagnosis  of  phthisis,  even 
though  the  hereditary  history  of  the  individual  be  against 
such  development.  If  there  be  a  slight  flattening  under  one 
clavicle,  with  marked  loss  of  expansion,  dulness  on  percus- 
sion, bronchial  respiration,  increased  vocal  resonance,  and 
an  abundance  of  crackling  rales  of  large  and  small  size, 
attended  by  a  fully  developed  phthisical  history,  however 
the  disease  may  have  commenced,  you  may  be  certain  of 
the  existence  of  phthisis. 

Never  attempt,  during  the  early  stage  of  phthisis,  to  make 
a  positive  diagnosis  as  to  the  state  of  the  lungs,  when  there 
has  been  a  recent  haemoptysis.  Attach  very  little  impor- 
tance to  slight  changes  in  respiration,  unless  they  are  ac- 
companied by  abnormal  percussion-sounds.  Never  give  a 
positive  opinion  in  a  doubtful  case  from  a  single  examina- 
tion ;  in  such  a  case,  at  your  different  examinations,  care- 
fully compare  the  local  signs  with  the  constitutiona) 
symptoms. 


LECTURE     XXII. 


PULMONABY  PHTHISIS 


Prognosis.  — Treatment. 

As  we  continue  the  history  of  phthisis,  the  subject  of 
prognosis  will  next  engage  our  attention. 

There  is  a  general  impression,  both  in  and  out  of  the 
profession,  that  an  individual  with  phthisis  is  doomed  to 
die  within  a  limited  period  of  time.  Unquestionably,  a 
large  majority  of  cases  terminate  fatally,  yet  improvement 
is  possible  in  all  stages  of  the  disease ;  approximate  re- 
covery may  take  place  in  more  than  one-half  the  cases, 
and  complete  recovery  is  not  infrequent. 

PKOGNOSIS  depends  very  much  upon  the  variety  and 
stage  of  the  phthisis.  In  cases  of  tubercular  phthisis  it  is 
always  unfavorable.  These  generally  terminate  fatally 
within  five  or  six  months  after  their  commencement.  In 
catarrhal  phthisis  the  prognosis  depends  almost  entirely 
upon  the  condition  of  the  patient  at  the  time  of  the  attack. 
If  the  affected  lung  is  in  the  first  stage  of  the  disease,  and 
the  amount  of  consolidation  is  moderate  in  extent,  the 
chances  for  the  arrest  of  the  phthisical  processes  are  cer- 
tainly promising,  and  it  is  possible  for  recovery  to  take 
place  in  at  least  one-third  of  the  cases. 

In  fibrous  phthisis  complete  recovery  rarely  if  ever  occurs, 
but  patients  with  this  disease  usually  live  many  years,  even 
to  old  age,  so  that  as  regards  duration  of  life  the  prognosis 
is  good.  You  can  hope  for  complete  recovery  only  in  ca- . 


262  PROGNOSIS. 

tarrhal  plithisis,  and  in  this  variety  only  in  the  first  stage 
of  the  disease,  and  when  there  has  been  no  extensive  con- 
solidation. 

If  a  patient  with  any  form  of  phthisis,  at  some  former 
period  in  his  history  has  suffered  from  phthisical  develop- 
ments, from  which  apparently  he  entirely  recovered,  his 
chances  of  recovery  from  a  second  phthisical  development 
are  lessened  by  this  first  attack.  Phthisical  symptoms  oc- 
curring in  early  life  render  the  prognosis  unfavorable  when 
phthisical  developments  come  on  in  middle  life. 

In  any  stage  of  phthisis  the  prognosis  may  be  rendered 
unfavorable  by  the  development  of  complications,  such  as 
the  occurrence  of  capillary  bronchitis,  pulmonary  oedema 
and  congestion  in  portions  of  lung  not  involved  in  the 
phthisical  process.  The  development  of  chronic  laryngitis 
is  a  serious  complication  in  phthisis,  and  when  it  causes  such 
extensive  changes  in  the  larynx  as  to  give  rise  to  complete 
aphonia,  the  difliculty  in  deglutition  which  attends  it,  and 
the  increased  irritation  produced  by  the  coughing,  so  wears 
out  the  patient  as  to  greatly  hasten  the  fatal  termination. 
Its  occurrence  in  connection  with  different  varieties  of  phthi- 
sical development  in  the  lungs  must  render  the  prognosis 
unfavorable. 

Pneumothorax  may  complicate  any  stage  of  phthisis,  but 
it  more  frequently  occurs  in  the  latter  stages.  Whenever  it 
does  occur,  it  is  of  exceedingly  grave  import,  such  cases 
usually  terminating  fatally  within  three  weeks  from  the 
time  of  its  occurrence. 

Profuse  hemorrhages  from  the  lungs  occurring  in  the  lat- 
ter stages  of  phthisis  render  the  prognosis  unfavorable  ;  the 
patient  may  partially  rally  from  the  effects  of  the  hemor- 
rhages, but  usually  a  more  rapid  destruction  of  lung-tissue 
follows  the  hemorrhage,'1  or  the  patient  soon  sinks  and  dies 
in  a  condition  of  asthenia. 

Diarrhoea  may  be  the  direct  cause  of  death  in  phthisis,  by 
contributing  to  a  more  complete  development  of  asthenia 
than  already  existed.  The  occurrence  of  a  profuse  and 
persistent  diarrhoea  in  the  advanced  stage  of  the  disease, 
therefore,  renders  the  prognosis  immediately  unfavorable ; 


PULMOjSTAKY   PHTHISIS.  203 

patients  with  pulmonary  phthisis  usually  die  from  asthenia, 
and  whatever  contributes  to  produce  that  condition,  con- 
tributes to  an  unfavorable  prognosis  more  or  less  immediate, 
according  to  the  severity  of  the  agent  which  produces  the 
asthenia. 

Occasionally,  patients  in  an  advanced  stage  of  phthisis 
die  from  syncope — a  simple  loss  of  power  in  the  heart  to 
perform  its  work. 

When  cedema  of  the  feet  and  legs,  due  either  to  throm- 
bosis of  the  veins  of  the  lower  extremities,  or  to  inter- 
current  structural  changes  in  the  kidneys,  comes  on  in 
advanced  phthisis,  the  prognosis  is  very  unfavorable ;  the 
oedema  usually  precedes  the  fatal  issue  only  by  a  few 
weeks. 

These  are  some  of  the  principal  complications  which  affect 
the  question  of  prognosis  in  phthisis.  There  is  no  general 
law  which  can  be  applied  to  all  cases  ;  each  one  has  its  own 
peculiar  history,  which  can  rarely  be  foretold  at  the  com- 
mencement of  the  disease  ;  you  cannot  evert  judge  accurately 
of  its  probable  duration.  The  general  condition  of  the 
patient,  the  rapidity  of  the  emaciation,  the  pulse  and  tem- 
perature, the  evidence  of  more  or  less  extensive  consolida- 
tion, .the  age  of  the  patient,  and  the  knowledge  of  the 
progress  of  the  disease  in  other  members  of  the  family,  as 
well  as  the  character  of  the  phthisical  processes,  may  give 
you  some  idea  of  the  probable  progress  of  the  disease. 
When  phthisis  has  existed  for  some  time,  you  may  judge 
something  of  the  future  by  knowing  the  past  history — at 
least  you  can  determine  to  what  extent  the  vital  powers  of 
the  patient  are  withstanding  the  ravages  of  the  local  disease  ; 
but  never  allow  yourself  to  give  a  positive  opinion  as  to  the 
duration  of  life.  Cases  that  appear  to  be  progressing  favor- 
ably, sudden' y  exhibit  unfavorable  symptoms,  and  those 
which  seem  very  near  their  termination,  unexpectedly  im- 
prove. 

Remember  that  a  phthisical  patient,  who  has  no  symp- 
toms that  are  immediately  alarming,  may  suddenly  develop 
a  pleurisy  with  a  copious  purulent  effusion,  a  pneumo- 
thorax,  a  peritonitis,  intestinal  ulceration,  a  severe  hsemop- 


!i>64  TREATMENT. 

tysis,  a  capillary  bronchitis,  pulmonary  oedema,  or  a  gen- 
eral tuberculosis,  the  occurrence  of  any  one  of  which  will 
completely  change  your  opinion  as  to  the  probable  du- 
ration of  life.  Whereas,  on  the  other  hand,  a  case  of 
phthisis  that  apparently  presents  all.  those  symptoms  which 
indicate  a  rapidly  fatal  termination,  suddenly  seems  to  be 
arrested  in  its  downward  course,  a  retrogressive  process  is 
established,  and  the  patient,  after  a  time,  reaches  a  condi- 
tion of  partial,  if  not  of  complete  recovery— at  least  he 
becomes  able  to  attend  to  the  ordinary  business  of  life ; 
especially  is  this  likely  to  occur  if  the  retrograde  process 
is  commenced  before  the  phthisis  passes  beyond  its  first 
stage. 

TREATMENT. — In  order  to  have  intelligent  views  in  regard 
to  the  management  of  phthisis,  you  must  constantly  bear 
in  mind  the  different  anatomical  changes  which  occur  in  its 
different  varieties,  as  well  as  the  different  causes  which  lead 
to  its  development. 

I  shall  consider  this  part  of  its  history  under  three  heads. 

First. — ITS  PROPHYLACTIC  TREATMENT. 

Second. — ITS  MEDICINAL  TREATMENT. 

Third. — ITS  HYGIENIC  TREATMENT. 

It  is  during  the  period  when  prophylactic  measures  can 
be  employed  that  we  have  the  greatest  power  in  controlling 
this  disease,  and  may  hope  to  obtain  the  most  satisfactory 
results. 

If  a  person  with  a  delicate  constitution,  having  a  tendency 
to  phthisical  development,  either  hereditary  or  acquired, 
commences  to  emaciate,  lose  strength,  and  furnish  other 
evidences  that  there  is  more  or  less  interference  with  healthy 
nutrition,  it  becomes  all-important  that  such  a  person  should 
be  immediately  placed  under  those  influences  which  shall 
arrest  this  defective  nutrition,  and  tend  to  invigorate  the 
constitution,  hoping  thereby  to  counteract  these  morbid 
tendencies.  For  instance,  if  this  train  of  symptoms  is  de- 
veloped in  persons  whose  occupation  or  habits  of  life  com- 
pel them  to  spend  the  greater  part  of  their  time  within 
doors,  change  of  occupation  must  be  secured,  and  sedentary 
habits  broken  up.  If  an  individual  with  phthisical  tenden- 


PULMOoSTAKY    PHTHISIS.  265 


cies  is  living  in  a  locality  where  lie  is  subject  to  depressing 
influences  of  any  kind,  change  in  location  must  be  insisted 
on,  and  you  should  endeavor  to  place  him  under  those  in- 
fluences which  are  invigorating  in  character. 

The  same  general  indications  should  be  observed  in  re- 
gard to  children  born  of  phthisical  or  decrepid  parents. 
Phthisical  or  feeble  mothers  should  never  be  allowed  to 
nurse  their  own  children  ;  such  children  should  be  placed  on 
healthy  wet-nurses  during  infancy,  and  during  childhood 
should  be  fed  chiefly  upon  good  cow's  milk,  and  whenever 
they  manifest  any  scrofulous  developments,  the  greatest 
care  should  be  exercised  in  diet  and  hygiene.  Change  of 
climate  and  surroundings  is  often  of  great  importance  in  the 
prophylaxis  of  this  class  of  children.  Let  the  child  be  re- 
moved from  the  city  to  the  country,  not  remaining  in  any 
one  place  long  at  a  time.  I  know  of  no  such  powerful 
agent  in  arresting  phthisical  tendencies  in  childhood  as  sys- 
tematic physical  exercise  in  the  open  air ;  this  physical 
training  should  be  commenced  in  infancy  and  continued  un- 
til adult  life.  The  prophylactic  treatment  of  phthisis  also 
demands  that  all  those  influences  which  tend  to  the  devel- 
opment of  pulmonary  hypersemia  and  catarrh  of  the  bron- 
chial tubes,  shall  be  avoided.  Therefore,  persons  with 
phthisical  tendencies  should  not  be  allowed  to  breathe  an 
atmosphere  laden  with  dust  or  charged  with  poisonous 
vapors, — they  should  not  be  permitted  to  pass  suddenly 
from  an  atmosphere  of  extreme  cold  to  one  of  extreme  heat, 
or  the  opposite.  It  is  important  that  this  class  of  persons 
should  have  the  largest  amount  of  fresh  air,  not  only  dur- 
ing the  day,  but  also  during  the  night, — their  sleeping 
apartments  should  be  large  and  well  ventilated  ;  this  latter 
condition  is  important,  for  in  such  apartments,  air  charged 
with  noxious  gases  is  much  more  deleterious  than  under 
any  other  circumstances  during  the  twenty-four  hours ; 
crowded  rooms  should  be  carefully  avoided, — not  infre-. 
quently,  phthisical  developments  occur  as  the  result  of 
spending  a  few  hours  in  a  crowded  assembly  room,  when 
afterwards  the  individual  is  suddenly  exposed  to  the  influ- 
ence of  intense  cold.  In  these  cases  the  lungs  become  hyper 


266  TREATMENT. 

semic  from  the  influence  of  the  poisonous  gases  inhaled,  a 
bronchial  catarrh  follows,  which  is  obstinate  in  character, 
and  if  the  patient  has  a  hereditary  or  an  acquired  tendency 
to  pulmonary  phthisis,  such  a  catarrh  develops  a  broncho- 
pneumonia,  which  leads  to  a  phthisis  after  the  manner 
already  described.  It  is  also  important  that  this  class  of 
persons  should  avoid  extreme  physical  exertion,  such  as 
violent,  running  and  jumping,  or  any  other  violent  physical 
exercise,  for  such  exercise  may  be  the  exciting  cause  of 
pulmonary  hemorrhage.  Chilling  the  surface  is  to  be 
guarded  against  with  the  greatest  care,  and  flannel  should 
be  worn  next  the  skin  throughout  the  year. 

The  diet  should  be  simple,  but  of  the  most  nutritious 
quality,  and  should  be  taken  at  regular  intervals.  The 
quantity  of  food  taken  should  be  limited  only  by  the  power 
of  digestion,  and  the  number  of  meals  must  depend  not 
upon  any  strict  rule,  but  on  the  circumstances  of  each  pa- 
tient. It  is  far  better  for  this  class  of  patients  to  take  four 
or  even  five  light  meals  each  day,  such  as  the  stomach  is 
able  to  digest  without  any  sensation  of  weight  or  pain,  than 
two  or  three  heavy  meals  followed  each  time  by  a  sensation 
of  oppression. 

The  daily  use  of  alcoholic  stimulants  is  always  injurious 
to  persons  with  phthisical  tendencies.  They  should  be 
taken  only  when,  from  the  influence  of  some  depressing 
cause,  there  is  a  physical  demand  for  them, — after  extreme 
fatigue,  or  severe  exposure  to  cold,  a  moderate  amount  of 
alcoholic  stimulants  may  be  of  service. 

Every  catarrh  in  a  phthisical  subject,  however  slight, 
must  be  treated  with  the  greatest  care,  and  the  treatment 
must  be  continued  until  all  traces  of  the  catarrh  have  dis- 
appeared. If  it  shall  have  reached  the  smaller  bronchi,  the 
necessity  for  immediate  attention  becomes  imperative,  and 
the  individual  must  be  carefully  shielded  from  the  action  of 
any  new  irritation.  I  know  of  nothing  so  certain  to  assist 
in  the  removal  of  bronchial  catarrh  in  this  class  of  subjects 
as  a  change  in  climate.  If  the  individual  lives  among  the 
mountains,  let  him  go  to  the  sea-side  ;  if  at  the  sea-side,  let 
him  go  among  the  mountains ;  this  will  secure  not  only 


PULMONAKY   PHTHISIS.  267 

a  change  in  habits  of  life,  but  a  change  in  the  character  of 
the  air  to  be  breathed.  All  measures  adopted  under  the 
head  of  prophylactic  treatment  of  phthisis  have  one  ob- 
ject in  view,  and  that  is,  to  so  sustain  the  vital  powers  that 
the  individual  shall  not  become  susceptible  to  the  local 
causes  of  phthisis ;  whatever  measures  can  be  adopted  to 
secure  this  end,  are  the  measures  which  will  be  best  adapted 
to  the  prevention  of  the  disease. 

THE  MEDICINAL  TREATMENT  OF  PHTHISIS. — In  the  man- 
agement of  developed  phthisis,  the  worst  enemy  that  you  will 
have  to  encounter  is  fever.  Upon  this  depends  the  mani- 
festation of  almost  all  the  other  symptoms,  for  it  is  the  im- 
mediate cause  of  all  the  principal  phenomena  of  the  disease. 
By  the  rise  in  temperature  you  know  that  a  bronchitis  has 
become  a  broncho-pneumonia ;  by  a  still  greater  rise  in  tem- 
perature, that  the  products  of  such  a  pneumonia  are  becom- 
ing cheesy  ;  and  by  the  hectic  and  night-sweats,  that  soften- 
ing is  taking  place.  The  character  and  frequency  of  the 
pulse,  the  progress  of  the  emaciation,  the  loss  of  strength, 
the  dyspnoea,  and  the  other  distressing  and  characteristic 
symptoms  of  the  disease,  depend  to  a  very  great  extent  upon 
the  amount  of  fever  in  any  given  case.  It  will  be  found, 
upon  a  careful  examination  of  a  large  number  of  cases  of 
phthisis,  that  in  a  certain  proportion  of  cases  there  is  a 
steady  progress  of  the  disease  from  the  commencement  to 
the  end,  the  temperature  gradually  reaching  a  higher  rate 
as  the  disease  progresses.  In  certain  other  cases,  the  phthis- 
ical processes  become  stationary  for  a  time,  then  another 
period  of  development  is  ushered  in  by  the  exciting  in- 
fluences of  some  local  cause,  or  putrid  absorption  ;  the  pa- 
tient may  be  the  subject  of  several  such  periods  of  develop- 
ment, but  in  every  instance  their  appearance  will  be  marked 
by  an  elevation  of  temperature,  and  when  the  retrograde 
change  is  to  occur,  there  is  always  an  accompanying  fall  in 
temperature.  The  control  of  the  temperature  is  therefore 
all -important  in  the  management  of  the  disease.  The  med- 
icinal agent  which  I  have  found  to  be  the  most  reliable 
antipyretic  is  the  sulphate  of  quinine.  This  drug  has 
long  been  used  in  the  treatment  of  pulmonary  phthisis,  but 


268  TKEATMENT. 

it  lias  usually  been  administered  simply  as  a  tonic.  It  is 
for  this  reason,  I  believe,  that  in  the  profession  sufficient  im- 
portance is  not  attached  to  its  use  as  a  remedial  agent  in  the 
treatment  of  phthisis.  By  most  practitioners  it  is  regarded 
as  a  powerful  agent  in  the  arrest  of  night-sweats, — it  doubt- 
less has  great  power  in  this  direction,  but  the  night-sweats 
are  only  a  part  of  the  fever,  and  its  power  to  control  the 
one  comes  from  its  power  to  control  the  other.  When 
given  in  sufficiently  large  doses  to  reduce  temperature,  it 
will  at  the  same  time  diminish  the  frequency  of  the  pulse 
and  arrest,  for  a  time  at  least,  symptoms  which  result  from 
the  fever. 

In  many  cases  the  fever  cannot  be  controlled.  Quinine 
may  somewhat  modify  its  severity,  and  perhaps  for  a  time 
arrest  the  progress  of  the  disease  ;  this  is  more  likely  to  be 
the  case  after  the  disease  has  passed  the  first  stage.  When 
the  first  elevation  of  temperature  occurs,  quinine  rarely  fails 
to  control  the  fever.  The  average  quantity  necessary  to  ac- 
complish this  result  is  twenty  grains  per  day,  and  it  should 
be  administered  in  one  or  two  doses  ;  it  does  not  reduce  tem- 
perature when  given  in  small  and  frequently-repeated  doses. 
Determine  the  time  at  which  the  high  temperature  usually 
manifests  itself,  and  administer  a  large  dose  one  or  two 
hours  preceding  it.  This  is  to  be  done  without  reference  to 
time  of  day,  or  time  for  taking  food.  Its  administration 
should  be  continued  as  long  as  possible  without  producing 
cinchonism,  or  until  the  temperature  falls ;  after  the  tem- 
perature commences  to  fall,  the  size  of  the  dose  may  be 
diminished.  If  the  temperature  rises  again,  the  dose  of 
quinine  must  be  increased,  and  when  it  falls  again,  it  may 
be  diminished.  With  careful  instruction  an  intelligent 
patient  may  become  his  own  observer,  and,  to  a  certain 
extent,  his  own  medical  attendant.  If  you  are  able  to  con- 
trol the  fever  by  this  agent,  in  very  many  instances,  by  the 
additional  beneficial  influences  of  a  change  of  climate,  you 
may  carry  your  patient  on  to  complete  recovery  ;  or,  if  not 
to  complete  recovery,  a  prolongation  of  life  may  be  ex- 
pected, and  the  patient  placed  in  a  comfortable  condition. 
In  some  cases,  even  when  cavities  exist  in  the  lungs,  phthi- 


PULMONARY  PHTHISIS.  269 

Bical  patients  may  be  very  much  improved  by  the  judicious 
administration  of  quinine.  Its  action  is  not  tonic,  but  anti- 
pyretic. As  the  result  of  personal  observation  and  ex- 
perience, I  am  conhdent  that  no  drug  has  equal  power  with 
quinine  in  arresting  phthisical  process  in  the  early  stage  of 
catarrhal  phthisis;  it  not  only  arrests  the  progress  of  the 
bronchial  catarrhs  which  precede  the  phthisical  develop- 
ments, but  to  a  very  great  extent  limits  the  morbid  processes 
within  the  alveoli.  In  tubercular  phthisis  it  has  little,  if 
any,  control  over  the  fever. 

In  fibroid  phthisis,  its  use  is  only  indicated  during  those 
slight  attacks  of  febrile  excitement  which  attend  its  pro- 
gress. 

Another  medicinal  agent  which  has  been  extensively  em- 
ployed in  the  treatment  of  phthisis,  and  which,  for  the  past 
twenty  years  has  enjoyed  the  reputation  of  curing  the 
disease,  is  cod-liver  oil.     It  has  been  claimed  that  if  the 
use  of  this  remedy  is  commenced  very  early  in  the  disease, 
it  has  the  power  of  arresting  the  progress  of  phthisical 
developments.     I  am  not  among  those  who  advocate  its 
indiscriminate  use.     I  doubt  if  it  exerts  any  specific  in- 
fluence upon  the  disease  ;  it  is  more  than  probable  that  all 
its  beneficial  influence  is  due  to  the  fact  that  it  furnishes 
some  element  essential  to  the  digestion  and  assimilation  of 
certain  nutritive  elements  of  the  food.     In  very  many  cases 
the  exact  manner  in  which  it  acts  remedially  is  not  well 
understood.     There  are  three  facts  which  seem  to  me  to 
afford  some  clue  to  the  mode  of  its  action.     First  unless 
the  patient  gains  in  weight  while  using  the  oil,  tt  seldom  or 
never  proves  remedial ;  second,  flesh  and  weight  may 
gained  during  its  administration,  and  still  the  phthisical 
processes  steadily  progress ;   third,  when  it  does  act  re- 
medially,  the  weight  gained  is  far  greater  than  would 
result  from  the  oil  as  a  mere  element  of  nutrition.     A  great 
gain  in  weight  will  sometimes  immediately  follow  the  ad 
ministration  of  a  small  quantity  of  oil. 

It  always  acts  remedially  with  more  certainty  in  young 
persons  and  children  than  in  the  aged;  generally,  old  per- 
Bons  are  not  very  much  benefited  by  its  use.  For  these 


270  TREATMENT. 

reasons,  and  many  more  of  similar  character,  it  seems  to  me 
that  when  it  acts  remedially,  it  aids  digestion  by  supplying 
some  element  which  is  essential  to  the  assimilation  of  food, 
and  the  establishment  of  healthy  nutrition ;  exactly  what 
this  element  is,  is  not  known ;  but  it  is  known  that  it  acts 
in  some  other  manner  than  simply  as  a  nutrient.  Those  pa- 
tients who  are  benefited  by  its  use  take  more  food  than 
they  have  been  accustomed  to  previous  to  its  employment, 
and  digest  it  more  readily.  In  some  instances,  diarrhoea 
will  be  arrested  by  its  use,  also  the  vomiting  of  food  after 
eating  ;  in  other  cases,  the  oil  itself  will  be  rejected,  and  its 
administration  rendered  impossible. 

There  are  certain  points  of  practical  importance  in  regard 
to  the  mode  of  administering  cod-liver  oil,  concerning  which 
I  will  say  a  few  words. 

If  possible,  it  should  be  given  in  connection  with  an  alkali. 
At  first,  only  small  doses  should  be  given,  not  often  repeated. 
A  teaspoonful  once  or  twice  a  day  is  sufficient  to  commence 
with,  the  dose  being  gradually  increased  to  a  table- spoonful 
three  times  a  day ;  no  special  benefit  is  to  be  derived  from 
the  administration  of  large  doses.  Most  patients  take  the 
oil  best  immediately  or  soon  after  meals.  If  it  disagrees 
with  the  stomach,  lying  down  for  a  short  time  after  taking 
it  will  often  prevent  any  disagreeable  sensation ;  some  can 
better  take  it  upon  going  to  bed  at  night.  Do  not  adminis- 
ter it  in  connection  with  stimulants,  unless  the  patient  can- 
not take  it  in  any  other  way. 

Regularity  and  perseverance  in  the  use  of  oil  is  essential 
in  order  to  obtain  the  full  benefit  it  is  capable  of  producing. 
If,  at  times,  it  seems  to  disagree  with  the  digestive  organs, 
it  may  be  temporarily  omitted,  especially  during  the  sum- 
mer months. 

The  best  oil  in  the  market  is  "Moller's,"  or  what  is  term- 
ed the  Norwegian  oil. 

Several  substances  have  been  recommended  as  substitutes 
for  cod-liver  oil,  such  as  glycerine,  cream,  extract  of  malt, 
pancreatic  emulsion,  koumiss,  etc.,  but  they  are  all  far  less 
efficacious  than  the  oil,  and  are  only  to  be  employed  when 
the  oil  does  not  act  ictnedially,  or  is  not  well  borne  by  the 


PULMO^AEY   PHTHISIS  271 

patient.  In  tubercular  phthisis,  when  there  is  high  fever 
and  a  rapid  pulse,  cod-liver  oil  is  not  usually  retained  by  the 
stomach,  and  if  it  is,  the  progress  of  the  disease  is  not  influ- 
enced by  it.  Under  such  circumstances,  its  administration 
should  not  be  insisted  upon. 

On  chemical  grounds  the  hypophosphates  of  lime  and 
soda  have  been  recommended.  It  has  been  claimed  that 
they  hasten,  or  at  least  contribute  to,  the  calcareous  trans- 
formation of  the  phthisical  nodules  ;  so  far  as  my  experience 
goes,  I  am  satisfied  that  these  remedies  are  serviceable  only 
when  intestinal  digestion  is  imperfect;  then  they  often  are 
of  great  service. 

Iron  will  be  of  service  in  the  treatment  of  phthisis  only 
when  fever  is  absent.  First,  reduce  the  temperature  ;  when 
that  has  been  effected,  administer  some  preparation  of  iron, 
especially  if  the  patient  is  in  a  condition  of  anaemia.  If  it 
is  administered  when  fever  is  present,  it  will  disturb  the 
digestion,  and  very  likely  cause  diarrhoea.  It  should  be 
administered  only  at  the  time  of  taking  food.  I  believe  iron 
by  hydrogen  is  by  far  the  most  serviceable  preparation  to  be 
employed.  Its  daily  administration  should  be  continued 
for  a  long  time. 

Inhalations  of  various  volatilizable  substances  have  been 
employed  in  the  treatment  of  phthisis,  but,  so  far  as  I  know, 
without  affording  any  permanent  relief. 

The  inhalation  of  the  vapor  of  warm  water  impregnated 
with  narcotic  extracts  relieves  laryngeal  irritation  and  pal- 
liates cough  ;  but  the  relief  afforded  is  not  permanent,  and 
the  vapor  does  not  act  remedially. 

Inhalations  of  tar,  creosote,  carbolic  acid,  iodine,  and  bal- 
sams, combined  with  sedative  extracts,  sometimes,  in  the 
early  stage  of  the  disease,  appear  to  produce  a  remarkable 
improvement  in  the  precursory  bronchial  catarrh,  but  they 
have  no  such  beneficial  effect  in  fully  developed  phthisis. 

My  experience  is  positively  against  the  use  in  phthisis  oi 
oxygen,  hydrogen,  or  nitrous  oxide  gas ;  they  seem  to  me 
to  increase  rather  than  retard  phthisical  developments. 

Although  it  has  been  claimed  that  the  inhalation  of  medi- 
cinal substances,  vapors,  and  gases  have  the  power  to  con- 


272  TREATMENT. 

trol  phthisical  developments,  yet  there  is  no  evidence  that 
such  is  the  case  ;  while,  on  the  other  hand,  there  is  positive 
evidence  that  they  do  harm  by  causing  the  development  of 
peribronchitis. 

Topical  applications  to  the  larynx  in  the  treatment  of 
the  laryngeal  affections  in  phthisis  have  already  been  con- 
sidered under  the  head  of  chronic  laryngitis.  Their  judi- 
cious use  in  many  cases  will  be  followed  by  very  great 
relief ;  it  is  important  that  such  intra-laryngeal  applications 
should  only  be  made  in  connection  with  the  laryngoscope, 
and  by  one  who  is  familiar  with  such  applications. 


LECTURE    XXIII. 


PULMONARY  PHTHISIS. 


Treatment.    (Continued.} 

I  SHALL  this  morning  continue  the  subject  of  the  medici- 
nal treatment  of  pulmonary  phthisis.  We  now  come  to  the 
use  of  alcohol  in  its  treatment.  There  is  a  great  diversity  of 
opinion  in  the  profession  as  regards  its  use  in  the  treatment 
of  phthisis.  Some  claim  for  it  a  curative  power,  others 
maintain  that  its  daily  use  does  harm.  The  question  there- 
fore arises,  under  what  circumstances  has  experience  taught 
us  that  it  is  of  service,  and  when  is  it  hurtful. 

I  am  convinced  that  benefit  may  be  expected  from  the  use 
of  alcoholic  stimulants  only  when  they  increase  the  desire 
for  food  and  assist  digestion,  or  when  their  use  is  followed 
by  a  feeling  of  increased  strength,  and  a  disposition  to  take 
exercise.  On  the  other  hand,  if  their  use  causes  a  rise  in 
temperature,  and  an  acceleration  of  the  pulse,  followed  by  a 
feeling  of  increased  weakness  and  nervous  depression,  they 
certainly  will  do  no  good,  and  probably  will  do  harm. 

The  idea  that  alcohol  has  the  power  of  arresting  phthisi- 
cal developments  is  one  which  experience  does  not  sustain. 
The  daily  use  of  alcohol  may  mask  for  a  time  the  phthisical 
symptoms,  and  the  patient  and  his  friends  may  fancy  that 
the  progress  of  the  disease  is  stayed  ;  but  soon  he  reaches  a 
condition  when  it  is  apparent  that  large  doses  of  stimulants 
are  not  arresting  its  progress. 

It  is  exceedingly  unfortunate  for  a  phthisical  patient  to 
become  addicted  to  the  daily  use  of  stimulants,  and  my  im- 

18 


274  TREATMENT. 

pression  is,  that  generally  phthisical  patients  do  better  with- 
out stimulants  than  with  them ;  especially  is  this  the  case 
in  the  earlier  stages  of  the  disease. 

If  an  individual  with  developed  phthisis  reaches  complete 
recovery  while  taking  alcoholic  stimulants  freely,  I  am  con- 
fident that  he  would  have  reached  it  more  rapidly  and  safely 
without  their  use. 

If  you  decide  to  administer  alcohol  in  phthisis,  the  quan- 
tity and  form  of  the  stimulant  to  be  used  must  be  deter- 
mined by  its  effects  ;  no  rule  can  be  given  for  its  adminis- 
tration, each  case  is  a  rule  unto  itself.  Malt  liquors  and 
wines  do  less  harm  than  whiskey  and  brandy,  and  are  usu- 
ally more  serviceable. 

Cough-mixtures  are  prescribed  by  physicians  to  phthisi- 
cal patients,  perhaps  more  frequently  than  any  other  medi- 
cinal agent.  Their  administration  will  eventually  be  fol- 
lowed by  injurious  effects.  Cough-mixtures  are  usually 
composed  of  substances  which  are  more  or  less  nauseating  ; 
and  as  the  future  well-being  of  every  phthisical  patient  de- 
pends upon  his  powers  of  digestion,  avoid  as  far  possible 
everything  which  may  interfere  with  the  healthy  action  of 
the  digestive  organs.  Although  you  may  temporarily  re- 
lieve a  distressing  symptom  by  a  cough-syrup,  still  by  its  ad- 
ministration you  will  cause  digestive  disturbance  which  will 
do  positive  harm  to  your  patient.  The  relief  obtained  by 
cough-mixtures  is  undoubtedly  due,  for  the  most  part,  to 
the  opium  which  they  contain,  and  this  brings  us  to  the  ques- 
tion, Should  opium  be  given  to  phthisical  patients  ?  In  an- 
swer to  this  question,  I  would  say  opium  should  never  be 
given  in  any  stage  of  phthisis,  unless  the  cough  is  distress- 
ing, and  the  patient  is  unable  to  obtain  the  requisite  amount 
of  sleep.  Under  such  circumstances  the  milder  anodynes 
should  first  be  tried.  If  possible  reserve  the  opium  for  the 
later  stages  of  the  disease.  Always  begin  its  use  with  the 
smallest  dose  that  will  give  rest. 

In  the  majority  of  instances  I  have  found  that  phthisical 
patients  obtain  more  speedy  and  satisfactory  relief  from 
their  cough  and  restlessness  by  the  inhalation  of  a  few  drops 
of  chloroform,  than  from  the  use  of  opium;  besides,  the 


PULMONARY  PHTHISIS.  275 

chloroform  is  less  liable  than  the  opium  to  disturb  the  pro- 
cess of  digestion.  You  must  be  watchful  of  your  patients 
as  regards  the  use  of  chloroform ;  there  is  danger  that  they 
may  become  addicted  to  its  excessive  use.  It  must  be  re- 
membered that  all  anodyne  remedies  act  in  a  similar  way, 
simply  as  palliatives  ;  they  should  only  be  employed  when 
the  symptoms  become  sufficiently  distressing  to  demand 
their  use. 

In  those  cases  where  a  constant  hacking  or  a  violent  par- 
oxysmal cough  is  excited  or  kept  up  by  an  inflamed  or 
irritable  condition  of  the  fauces,  the  topical  application  of 
anodynes  or  astringent  remedies  by  means  of  sprays  or  a 
camel'  s-hair  brush  will  often  be  found  of  great  service. 

Counter-irritants  to  the  surface  of  the  chest  have  always 
been  regarded  as  very  important  in  the  treatment  of  phthisis ; 
it  is  the  common  practice  to  employ  them  in  all  stages 
of  the  disease.  The  pain  in  the  chest  for  the  relief  of  which 
they  arc  generally  employed  I  have  already  stated  to  you 
depends  upon  two  distinct  causes — namely,  a  neuralgic 
affection  of  the  intercostal  nerves,  and  localized  pleuri- 
sies ;  the  former  is  best  relieved  by  the  application  of  cold 
or  warm  compresses  over  the  seat  of  pain,  the  latter  by  dry 
cups  or  small  blisters. 

My  impression  is  that  all  the  liniments  and  plasters  so 
frequently  employed  in  this  class  of  cases  are  objectionable, 
as  they  interfere  with  cutaneous  function  over  a  large  sur- 
face without  affording  any  permanent  relief. 

Croton-oil  and  tartar-emetic  applications  as  means  for 
producing  counter-irritation  are  at  least  of  doubtful  utility, 
while  they  give  the  patient  much  discomfort.  In  a  catarrhal 
phthisis,  when  a  bronchial  catarrh  is  passing  into  a  broncho- 
pneumonia,  dry-cupping  is  generally  the  most  serviceable 
counter-irritant.  After  the  broncho-pneumonia  has  become 
established  the  greatest  benefit  will  be  derived  from  the  use 
of  blisters,  small  in  size,  applied  directly  over  or  in  the 
region  of  the  pulmonary  consolidation. 

Dry  friction  to  the  surface  of  the  chest  by  means  of  coarse 
flannel  or  a  flesh-brush  will  often  give  entire  relief  from  those 
pains  which  are  due  to  neuralgic  affections  of  the  inter- 


276  TREATMENT. 

costal  spaces ;  it  should  be  employed  regularly  morning  and 
evening. 

Gastric  and  intestinal  disturbances  are  a  part  of  the  his- 
tory of  nearly  every  case  of  phthisis,  and  there  are  two  con- 
ditions upon  which  the  diarrhoea  and  distress  after  eating 
depend.  They  may  depend  upon  a  hypersemic  condition  of 
the  gastro-intestinal  mucous  membrane  produced  by  indi- 
gestible food,  or  the  diarrhoea  may  depend  upon  ulceration 
of  the  large  or  small  intestines.  If  it  depend  upon  gastro- 
intestinal hypersemia,  the  result  of  irritation  produced  by 
indigestible  food,  the  quantity  and  quality  of  the  food  must 
be  carefully  attended  to.  and  a  mild  saline  laxative  rather 
than  an  astringent  must  be  administered;  this  should  be 
followed  by  the  daily  use  of  the  lacto-phosphate  of  lime. 
If  the  diarrhoea  is  dependent  upon  ulcerations  existing  in 
the  small  intestines,  the  administration  of  cod-liver  oil  and 
the  hypophosphates  of  lime  and  soda  will  be  of  service.  If 
these  fail  to  give  relief,  ten  grains  of  bismuth,  combined 
with  a  twelfth  of  a  grain  of  morphine,  given  after  each 
movement,  will  almost  certainly  control  the  diarrhoea.  If 
the  diarrhoea  depends  upon  ulceration  of  the  large  intestines 
(the  presence  of  blood  in  the  discharges  being  regarded  as 
an  evidence  of  these  ulcerations),  all  that  can  be  done  is  to 
give  temporary  relief  by  opium  suppositories. 

Vomiting  after  meals  is  often  a  troublesome  attendant  of 
phthisis.  When  it  occurs  in  tubercular  phthisis,  it  is  rarely 
permanently  relieved.  Champagne  with  the  food,  hydro- 
cyanic acid,  pepsin,  and  a  long  list  of  remedies  are  recom- 
mended for  its  relief.  The  most  certain  relief  is  obtained  by 
compelling  the  patient  to  take  every  half  hour  for  forty- 
eight  hours  from  one-half  to  one  teaspoonf ul  of  raw  scraped 
beef  made  into  a  sandwich,  at  the  same  time  keeping  him 
absolutely  quiet  in  a  recumbent  posture. 

Night- Sweats. — These  usually  occur  in  the  advanced  stage 
of  phthisis,  but,  as  I  have  already  told  you,  they  may  occur 
in  an  early  stage  of  the  disease.  They  often  occur,  disap- 
pear, and  recur  without  any  apparent  cause.  They  are  a 
part  of  the  hectic,  fever,  and  if  you  fail  to  control  them  by 
large  doses  of  quinine,  a  combination  of  digitalis,  opium, 


PULMONARY   PHTHISIS.  277 

and  quinine  may  effect  the  desired  result.  Aromatic  sul- 
phuric acid,  oxide  of  zinc,  fluid  extract  of  ergot,  chloral, 
and  infusions  of  hops,  sage,  etc.,  have  been  recommended, 
and  at  times  will  be  found  of  service.  Sponging  the  surface 
of  the  body  at  night  with  warm  or  cold  water,  or  acidulated 
water,  I  have  found  very  grateful  to  this  class  of  patients. 
The  question  always  presents  itself  when  night-sweats  are 
profuse,  as  to  the  propriety  of  suddenly  arresting  them. 

The  medicinal  treatment  of  phthisis  resolves  itself  there- 
fore into  the  observance  of  a  few  general  principles,  and  not 
in  the  use  of  any  vaunted  or  specific  remedies. 

Human  ingenuity  has  been  exercised  to  its  utmost  extent 
in  attempts  to  formulate  prescriptions  for  the  cure  of  this 
disease,  but  as  yet  no  specific  remedy  has  been  found.  Cer- 
tain results  can  be  accomplished  by  the  administration  of 
certain  well-known  remedies,  sometimes  palliative  and  some- 
times apparently  curative ;  beyond  this,  the  intelligent  phy- 
sician cannot  safely  venture. 

THE  HYGIENIC  TREATMENT  OF  PHTHISIS. — Under  this  head 
are  included  some  of  the  most  important  agents  in  the  suc- 
cessful management  of  this  disease.  The  quantity  and 
quality  of  the  air  habitually  respired  is  the  first  and  most 
important  thing  to  be  considered.  If  it  is  anti-hygienic, 
your  first  effort  should  be  to  change  it.  Therefore,  if  a 
phthisical  patient  is  surrounded  by  an  atmosphere  contami- 
nated by  impurities  arising  from  decaying  animal  or  vege- 
table matter,  or  by  the  presence  of  noxious  gases,  his  location 
must  at  once  be  changed,  or  the  impurities  removed.  If 
possible,  phthisical  patients  should  spend  the  greater  part 
of  the  day  in  the  open  air ;  their  sleeping  apartments  should 
be  large,  well-ventilated  and  well-lighted,  and  should  be 
situated  on  the  southerly  and  westerly  side  of  the  building. 

As  a  rule,  the  windows  of  the  sleeping  apartments  should 
be  closed  during  the  night ;  if  the  rooms  are  not  sufficiently 
large  to  prevent  the  air  from  becoming  impure,  fresh  air 
may  be  admitted  from  an  open  window  in  an  adjoining 
room.  The  influence  of  air  overladen  with  carbonic  acid 
gas  upon  the  respiratory  organs  is  to  induce  pulmonary 
hypersemia,  and  thus  it  places  a  phthisical  patient  in  a  con- 


278  TKEATMEJST. 

dition  which  favors  the  development  of  bronchial  catarrh 
and  broncho-pneumonia. 

Great  care  should  be  exercised  in  the  management  of  all 
persons  with  developed  phthisis,  to  prevent  the  surface  of 
the  body  from  being  chilled.  Although,  as  I  have  already 
stated,  the  most  important  element  in  the  hygienic  manage- 
ment of  the  disease  is  fresh  air,  yet  great  discretion  must 
be  exercised  in  the  selection  and  adoption  of  means  which 
shall  secure  it,  lest  the  beneficial  effects  be  lost  by  the  inju- 
rious influences  to  which  the  patient  is  subjected.  To  rec- 
ommend that  every  day  a  patient  far  advanced  in  phthisis 
should  be  taken  into  the  open  air  is  unwise  ;  indeed,  in  any 
stage  of  the  disease,  if  the  patient  rides  or  walks  and  re- 
turns chilled  by  the  exposure,  it  is  far  better  for  him  to  re- 
main within  doors,  and  by  means  of  some  well-regulated 
and  non-exhausting  gymnastics,  take  physical  exercise  in  a 
large  well-ventilated  room.  Every  exposure,  when  the  vital- 
ity of  the  system  is  not  sufficient  to  keep  the  surface  of  the 
body  warm,  tends  to  render  the  pulmonary  tissue  hyperae- 
mic,  and  becomes  harmful  rather  than  beneficial. 

The  constitutional  peculiarities  of  each  patient  must  be 
carefully  studied  with  reference  to  everything  embraced 
under  the  head  of  hygienic  treatment.  The  same  general 
principles  with  reference  to  fresh  air  are  to  govern  you  in 
the  hygienic  treatment  of  phthisis  as  were  given  you  under 
the  head  of  its  prophylactic  treatment. 

With  regard  to  diet,  milk  seems  best  suited  to  this  class 
of  patients ;  asses'  milk  has  been  claimed  to  be  the  most  nu- 
tritious ;  goats'  milk  has  also  become  somewhat  popular  in 
the  treatment  of  phthisis,  especially  in  connection  with 
phthisical  manifestations  in  children  ;  yet  good  cows'  milk 
will  prove  sufficiently  nutritious  to  afford  all  the  benefit 
which  can  be  derived  from  a  milk  diet. 

Yolk  of  eggs,  combined  with  milk,  in  many  cases  will 
prove  exceedingly  beneficial.  In  some  cases  of  advanced 
phthisis,  this  combination  will  be  well  borne  when  no  other 
nutriment  can  be  taken. 

As  a  rule,  the  diet  of  phthisical  patients  should  be  most 
nutritious,  easy  of  digestion,  and  more  or  less  varied.  The 


PULMOTSTAKY   PHTHISIS.  279 

quantity  of  food  taken  should  be  limited  only  by  the  pow- 
er of  digestion.  The  number  of  meals  during  the  day  must 
not  be  restricted  to  three ;  five,  or  even  six  meals  often  may 
be  taken  with  benefit. 

The  question  of  climate  is  one  of  great  importance  in  the 
treatment  of  phthisis.  In  regard  to  this,  no  absolute  rules 
can  be  laid  down  ;  I  shall  therefore  confine  myself  to  a  few 
general  remarks. 

The  individual  peculiarities  of  each  case  must  decide  this 
question.  Experience  shows  that  one  individual  improves 
in  a  warm,  moist  air ;  another  individual  improves  in  a 
cold,  dry  air.  Every  phthisical  patient  has  a  climate  adapted 
to  his  peculiar  diathesis  ;  a  few  well-directed  questions  will 
enable  you  to  determine  in  which  direction  and  in  what 
locality  your  patient  will  be  most  likely  to  receive  benefit. 
In  the  first  place,  by  careful  questioning  determine  whether 
your  patient,  when  in  a  state  of  health,  was  most  vigorous 
in  warm  or  cold  weather,  in  a  damp  or  dry  atmosphere. 
Again,  you  must  determine  whether  he  has  most  vigor  in  a 
dry  and  cold,  or  a  dry  and  warm  atmosphere,  or  in  a  warm- 
moist,  or  cold-moist  atmosphere. 

If  these  questions  cannot  be  settled  by  the  experience  of 
the  patient,  direct  your  patient  to  travel  in  the  direction 
which  seems  best  suited  to  his  case,  until  he  finds  a  locality 
where  he  is  comparatively  comfortable,  endeavoring  to  select 
a  climate  where  he  may  be  out-of-doors  every  day,  and  at 
any  hour  of  the  day. 

Nearly  every  variety  of  climate  can  be  found  in  this 
country  ;  the  difficulty  is,  that  the  climatic  variations  have 
not  been  sufficiently  studied.  Besides,  in  very  many  in- 
stances, the  localities  which  are  best  suited  to  the  largest 
number  of  phthisical  patients  are  destitute  of  those  com- 
forts and  social  surroundings  which  are  so  important  to  the 
welfare  of  this  class  of  individuals. 

In  the  following  brief  summary  I  will  endeavor  to  give 
you  the  essential  climatic  conditions  and  variations  of  those 
localities  which  have,  at  different  times,  had  a  more  or  less 
extended  reputation  in  the  climatic  treatment  of  phthisis. 

When,  from  the  history  of  the  individual,  a  dry,  cold 


280  TREATMENT. 

atmosphere  is  indicated,  direct  your  patient  to  make  a  trial 
of  such  a  climate  as  that  of  Minnesota.  Its  winters  are  long 
and  cold,  the  spring  of  short  duration,  the  summer  is  very 
warm  (warm  days  and  cool  nights),  the  autumn  is  delight- 
ful, and  all  seasons  are  characterized  by  dryness  of  at- 
mosphere. Minnesota  is  situated  so  far  inland,  with  an 
annual  rainfall  (including  snow)  of  only  twenty -five  inches, 
that  its  climate  must  necessarily  be  dry.  There  are  sudden 
changes  of  temperature,  but  as  the  air  does  not  contain 
moisture,  their  effect  is  not  decidedly  injurious.  The  air 
is  dry  and  bracing.  The  country  has  an  elevation  above  the 
sea  of  one  thousand  feet,  in  some  portions  the  elevation  is 
much  higher.  In  addition,  the  land  is  covered  with  thick 
forests  of  spruce  and  pine. 

The  climate  is  not  remedial,  but  tonic — it  is  a  stimulating 
climate.  Let  none  go  to  Minnesota  who  are  unable  to 
exercise  in  the  open  air  ;  let  those  who  feel  better  at  home 
on  cold,  clear  days,  and  more  uncomfortable  on  warm, 
damp  days,  take  up  their  residence  there. 

The  climate  of  California  (especially  southern  California), 
Colorado,  certain  portions  of  Georgia,  South  Carolina,  etc., 
is  well  adapted  to  that  class  of  phthisical  patients  who  re- 
quire a  dry,  warm  atmosphere. 

In  sending  patients  to  California,  great  care  should  be  ex- 
ercised. The  experiences  of  the  individual  is  the  only  safe 
guide  in  the  choice  of  a  locality  best  suited  to  his  or  her 
case. 

The  climate  differs  in  the  different  sections.  The  heat  is 
much  greater  in  one  than  in  another,  and  the  rainfall  varies  ; 
in  one  it  may  be  about  twelve  inches,  in  another  twenty- 
four  inches.  In  many  portions  the  equability  of  temper- 
ature and  the  bracing  atmosphere  render  it  more  beneficial 
to  phthisical  patients  than  most  localities  in  this  country  or 
Europe.  Especially  is  this  true  of  Santa  Barbara.  It  has 
a  dry,  mild  climate  throughout  the  year,  and  is  not  subject 
to  sudden  changes  of  temperature.  The  rainfall  through- 
out the  year  is  only  from  twelve  to  fifteen  inches.  San, 
Diego,  San  Jose,  San  Bernardino,  and  many  other  places 
may  be  resorted  to  by  consumptives  with  great  benefit. 


PULMONARY   PHTHISIS.  281 

The  climate  of  Colorado  is  mild  and  peculiarly  dry,  from 
its  elevation ;  the  atmosphere  is  highly  exhilarating  and 
particularly  healthful.  Here  flowers  grow  at  the  height  of 
8,000  feet ;  usually  at  a  much  less  height,  vegetation  does 
not  flourish.  The  rainfall  for  one  year  was  about  sixteen 
inches.  In  some  sections  there  are  but  slight  variations  in 
temperature  throughout  the  year.  The  winter  days  are 
those  of  a  northern  summer,  and  the  summer  is  but  little 
wanner  than  the  winter. 

The  natural  parks  (scattered  throughout  this  region) 
afford  many  places  suitable  for  phthisical  invalids,  espe- 
cially the  Middle  and  South  Park. 

Throughout  Colorado  there  is  a  characteristic  clearnesa 
of  atmosphere  unlike  that  of  any  other  region  in  this  coun- 
try. Persons  in  the  incipient  stages  of  phthisis  do  well; 
but  the  air  is  so  thin  and  dry  that  it  is  very  likely  to  cause 
hemorrhages  in  those  cases  where  they  have  previously 
occurred. 

In  the  southern  portion  of  Georgia  the  atmosphere  is 
quite  mild  and  dry,  especially  in  the  vicinity  of  the  pine 
forests,  which  undoubtedly  have  very  much  to  do  with 
the  beneficial  effects  experienced  by  many  phthisical  sub- 
jects who  have  taken  up  their  residence  in  this  region. 
There  is  a  greater  rainfall  than  in  California  or  Colorado, 
and  the  country  is  more  often  visited  by  north-east  storms. 
At  Augusta  the  mean  winter  temperature  is  about  50°  F., 
and  in  the  more  southern  portion  of  the  State  it  is  even 
higher. 

Aiken,  in  South  Carolina,  is  situated  upon  a  sandy  eleva- 
tion, and  the  atmosphere  is  clear  and  mild,  with  an  even, 
warm  temperature.  In  its  vicinity  are  groves  of  pines. 
Cold  north-east  storms  are  prevalent.  The  three  spring 
months  are  best  suited  to  the  needs  of  phthisical  patients. 
Many  are  greatly  benefited  by  a  stay  in  Aiken. 

When  you  decide,  from  the  experience  of  a  phthisical 
patient,  that  a  warm,  moist  climate  is  required,  let  him  go 
to  the  Bermudas,  or  to  some  of  the  West  India  Islands,  or 
io  the  eastern  portion  of  Florida. 

The  climate  of  the  Bermuda  Islands  is  very  mild ;  the 


282  TREATMENT. 

mean  temperature  of  the  winter  months  is  60°  F.  They  are, 
however,  often  visited  by  south-west  storms,  which  are  cold 
and  disagreeable ;  the  prevailing  winds  are  from  the  west 
and  north-west.  The  weather  is  mild,  and  does  not  produce 
the  languor  of  other  atmospheres  nearer  the  tropics.  The 
air  is  generally  moist  and  warm,  from  the  influence  of  the 
Gulf  Stream. 

During  the  winter  the  weather  in  Nassau  (the  capital  of 
the  Bahamas)  is  mild,  clear,  and  invigorating;  it  has, 
usually,  a  moist,  warm,  but  very  healthy  climate.  Turk' s 
Island,  Santa  Cruz,  St.  Thomas,  etc.,  all  have  some  reputa- 
tion as  resorts  for  invalids. 

There  are  many  localities  on  the  island  of  Cuba  suitable 
for  a  home  for  phthisical  patients  during  the  winter  months, 
where  the  climate  is  mild  and  equable.  At  Matanzas  the 
atmosphere  is  dryer  than  at  Havana. 

The  climate  of  the  eastern  portion  of  Florida  is  warm  and 
moist ;  the  average  mean  temperature  for  1873  was  73°  F., 
with  a  variation  of  only  twenty-five  degrees.  The  rainfall 
is  forty  inches,  the  greatest  amount  is  during  the  summer. 
North-east  storms  occasionally  prevail.  At  St.  Augustine 
the  atmosphere  is  warm  and  moist,  with  but  slight  variations 
in  temperature  during  the  twenty-four  hours.  Along  the 
St.  John's  River,  at  Jacksonville,  Magnolia,  and  other 
towns,  there  is  less  moisture  than  at  St.  Augustine. 

Under  the  head  of  a  cool  and  moderately  moist  climate,  I 
know  of  no  region  that  my  experience  during  the  past  few 
years  of  its  effects  upon  phthisical  subjects  would  lead  me 
more  heartily  to  recommend  to  those  likely  to  be  benefited 
by  such  a  climate,  than  the  Adirondack  region,  situated  in 
the  northern  part  of  our  own  State. 

In  this  region,  during  the  summer  months,  the  minimum 
temperature  rarely  falls  below  50°  F.,  and  the  maximum 
rarely  reaches  70°  F.,  while  the  winters  are  cold  and  the 
temperature  equable.  Its  altitude  is  about  one  thousand 
seven  hundred  feet  above  sea-level. 

The  atmosphere  of  this  region  is  peculiarly  exhilarating : 
in  many  instances,  under  its  influence,  phthisical  bronchitis 
rapidly  disappears. 


PULMONARY   PHTHISIS.  283 

I  shall  not  detain  you  with  the  climatic  variations  of  the 
different  resorts  for  consumptives  on  the  continent  and  in 
other  foreign  countries,  for  these  have  all  been  very  fully 
considered  by  European  writers,  whose  personal  experience 
in  many  instances  furnishes  a  safe  guide  to  any  phthisical 
patient  who  may  prefer  a  foreign  residence  to  any  of  our 
home  resorts.  My  impression  is,  that  on  our  own  continent 
there  are  many  localities  far  better  adapted  to  the  different 
classes  of  phthisical  subjects  which  I  have  named  than  can 
be  found  in  any  other  portion  of  the  globe. 

The  climatic  treatment  of  phthisis  is  almost  exclusively 
confined  to  Us  first  stage.  In  the  last  stage  of  the  disease 
patients  will  do  far  better  to  remain  at  home  where  they  can 
be  surrounded  by  friends  and  the  luxuries  of  home-life,  than 
to  attempt  to  derive  benefit  from  changes  which  necessarily 
must  deprive  them  to  a  greater  or  less  extent  of  those  com- 
forts which  are  essential  to  the  well-being  of  the  weak  and 
feeble.  It  is  only  during  the  first  stage  of  the  disease  that 
any  permanent  arrest  of  its  development  can  be  expected, 
and  frequent  changes  of  climate  are  all-important  in  order  to 
accomplish  this  result. 

During  this  stage,  sometimes  patients  will  be  benefited 
by  a  long  sea-voyage  ;  many  persons  cannot  avail  themselves 
of  this  advantage,  yet  can  take  up  a  permanent  residence 
on  some  small  island  far  out  at  sea :  from  this  they  may 
derive  great  benefit. 

In  whatever  locality  a  phthisical  patient  finds  himself  im- 
proving, it  is  important  that  he  remain  in  that  locality  so 
long  as  he  continues  to  improve. 

Physical  exercise  is  another  essential  element  in  the  hygi- 
enic treatment  of  phthisis.  Unless  regular  and  systematic 
physical  exercise  is  taken,  all  other  hygienic  measures  will 
fail  to  accomplish  the  expected  beneficial  results.  Female 
phthisical  patients  are  always  weak  and  languid,  and  are 
unwilling  to  take  exercise  unless  forced  to  it ;  they  are 
easily  fatigued,  consequently  the  digestive  and  assimilative 
processes  are  interfered  with  to  such  an  extent  as  to  injure 
rather  than  benefit  the  patient.  In  these  cases  something 
may  be  accomplished  by  passive  exercise.  Physical  exer- 


284  TKEATMENT. 

else  should  never  be  carried  to  over-fatigue,  and  it  should 
always  be  taken  in  the  open  air  or  in  a  well- ventilated 
room. 

When  a  phthisical  patient  is  fond  of  out-of-door  sports, 
such  as  hunting  and  fishing,  the  chances  for  improvement 
in  his  case  are  far  better  than  if  such  sports  were  distasteful 
to  him. 


DISEASES    OF   THE   HEART. 


LECTURE    XXIV. 


DISEASES  OF  THE  HEART. 

Different  Forms. — Acute  Pericarditis. 

GENTLEMEN  : — I  shall  this  morning  commence  the  history 
of  cardiac  diseases,  a  class  of  diseases  which,  on  account  of 
their  frequency,  as  well  as  on  account  of  the  distressing 
phenomena  which  attend  their  development,  have  always 
particularly  engaged  the  attention  of  medical  men.  Yet  it 
is  only  since  the  discovery  of  auscultation  that  they  have 
been  diagnosticated  with  accuracy,  or  their  symptoms  de- 
scribed with  anything  like  precision. 

The  recent  advances  which  have  been  made  in  our  know- 
ledge of  the  physiology  and  histology  of  the  heart,  as  well  as 
the  new  interpretations  given  to  the  anatomical  changes  that 
take  place  in  it  during  the  development  of  its  different 
morbid  processes,  give  a  new  interest  to  the  study  of  this 
class  of  diseases.  Within  the  past  few  years,  a  revolution 
has  taken  place  in  cardiac  pathology  similar  to  that  which 
has  occurred  in  connection  with  the  pathology  of  many  of 
the  other  diseases  which  have  been  engaging  our  attention. 

I  have  grouped  the  different  forms  of  cardiac  diseases 
which  we  shall  now  study  under  the  following  heads : 

First.  —  PERICARDITIS,  WHICH  MAY  BE  ACUTE  OB 
CHRONIC. 

Second. — ENDOCARDITIS,    WHICH    MAY    BE   ACUTE    OR 

CHRONIC. 

Third. — VALVULAR  LESIONS. 
Fourth. — CARDIAC  HYPERTROPHY. 


£88  MORBID   ANATOMY. 

Fifth.— CARDIAC  DILATATION. 

Sixth.—  MYOCARDITIS,  WHICH  is  ALWAYS  SECONDARY. 

Seventh.—  DEGENERATION  OF  THE  WALLS  OF  THE  HEART, 

EITHER  FATTY   OR  WAXY. 

Mg7it7i.—A.TRO?&Y  OF  THE  WALLS  OF  THE  HEART. 

Ninth.—  THROMBOSIS  OF  THE  HEART. 

Tenth.—  ANEURISMS  OF  THE  HEART. 

Eleventh. — NEW  FORMATIONS,  CANCER,  TUBERCLE,  ETC. 

Twelfth. — NEUROSES,  OR  NERVOUS  AFFECTIONS  OF  THE 

HEART. 

Under  these  heads,  all  the  different  forms  of  cardiac  dis- 
ease may  be  included. 

I  shall  first  invite  your  attention  to  inflammation  of  the 
pericardium,  or  pericarditis. 

PERICARDITIS. 

Anatomists  tell  us  that  the  pericardium  is  composed  of  a 
fibrous  and  serous  layer;  that  the  fibrous  layer  is  firmly 
attached  to  the  diaphragm  and  encircles  the  large  vessels 
about  two  inches  above  the  heart ;  by  these  attachments  a 
closed  sac  is  formed.  The  serous  layer  closely  adheres  to 
the  internal  surface  of  the  fibrous  layer,  is  reflected  from 
the  large  vessels,  and  completely  invests  the  heart  itself. 
Thus  we  have  formed  a  shut  serous  sac,  and,  when  diseased, 
it  behaves  in  all  respects  like  the  pleura. 

Inflammation  of  the  pericardium  may  be  acute  or  chronic. 
Chronic  pericarditis  usually  is  the  sequelae  of  acute. 

ACUTE  PERICARDITIS. 

This  is  not  an  uncommon  affection,  and  is  perhaps  more 
frequently  overlooked  than  any  other  acute  disease,  for 
its  objective  symptoms  are  rarely,  if  ever,  well  marked. 

MORBID  ANATOMY. — The  morbid  anatomy  of  pericarditis 
in  nearly  all  respects  is  similar  to  that  of  pleurisy.  At  the 
commencement  of  the  inflammatory  process,  the  serous  sur- 
face of  the  pericardium  becomes  more  or  less  reddened, 
with  here  and  there  ecchymotic  spots  of  irregular  shape. 
The  reddening  may  be  circumscribed,  or  involve  the  whole 
extent  of  the  pericardium,  both  the  visceral  and  parietal 


ACUTE   PERICARDITIS.  289 

portion.  The  discoloration  may  be  intense,  and,  as  in 
pleurisy,  is  due  to  hypersemia  of  the  subserous  capillary 
vessels.  With  the  redness,  there  is  a  swelling  and  infiltra- 
tion, not  only  of  the  serous  tissue  of  the  pericardium,  but 
the  subserous  tissue  also  undergoes  a  certain  amount  of 
infiltration.  As  in  pleurisy,  following  the  hypersemia  and 
infiltration,  the  epithelial  covering  is  separated  and  thrown 
off  into  the  pericardial  sac.  This  causes  the  membrane  to 
lose  its  natural  glistening  appearance.  If  the  inflammatory 
action  is  continued,  and  exudation  is  poured  out  on  the 
free  surface  of  the  pericardium  and  into  the  pericardial  sac, 
the  exudations  are  similar  to  those  which  were  described  as 
occurring  in  pleurisy  ;  the  plastic  exudation  varies  very 
much  in  thickness,  and  may  accumulate  on  the  cardiac  and 
parietal  surfaces  of  the  pericardium,  or  only  on  the  car- 
diac, varying  in  thickness  from  a  line  to  three-fourths  of  an 
inch,  or  may  have  even  a  greater  thickness.  As  soon  as 
the  plastic  material  is  poured  out,  it  causes  the  serous  sur- 
face of  the  pericardium  to  present  a  roughened  appearance  ; 
it  is  this  appearance  which  has  given  rise  to  the  expression 
"hairy  heart." 

The  fluid  effusion  which  we  have  in  pericarditis  is  vari- 
able in  quantity  and  quality.  It  may  be  sero-albuminous, 
sero-fibrinous,  hemorrhagic,  or  purulent ;  a  purulent  exuda- 
tion in  pericarditis  is  of  rare  occurrence. 

The  quantity  of  the  fluid  varies  from  three  to  twelve 
fluid  ounces.  In  most  instances  the  fluid  effusion  will 
be  sero-fibrinous  in  character ;  it  is  rarely  sero-albumi- 
nous. 

When  there  is  only  a  very  small  amount  of  plastic  exu- 
dation, usually  it  will  be  found  on  that  portion  of  the  peri- 
cardium which  covers  the  blood-vessels ;  hence,  a  friction- 
sound  may  be  heard  at  the  upper  portion  of  the  precordial 
space,  and  at  no  other  point  will  there  be  evidences  of  peri- 
cardial inflammation. 

When  the  fluid  effusion  is  small  in  amount,  it  will  grav- 
itate to  the  most  depending  portion  of  the  pericardial  sac. 
When  it  is  large  in  quantity,  the  entire  pericardial  sac  is 
filled,  and  the  adjacent  lung-tissue  compressed. 

19 


290  MORBID   ANATOMY. 

As  in  pleurisy,  so  in  pericarditis  these  exudations  and 
effusions  may  all  undergo  absorption.  The  serous  effusion 
is  removed  rapidly, — the  hemorrhagic  with  less  facility,  — 
the  plastic  and  purulent  with  still  greater  difficulty. 

The  lymph  and  purulent  exudations  may  undergo  fatty 
metamorphosis  and  be  absorbed,  or  remain  in  a  cheesy, 
mortar-like  mass,  and  finally  become  calcareous  after  the 
absorption  of  the  more  fluid  portion  of  the  degenerated 
mass.  The  calcareous  material  with  connective-tissue  for- 
mations may  form  ossified  plates  upon  the  surface  of  the 
heart  and  pericardium. 

The  tissue  of  the  pericardium  undergoes  the  same  changes 
that  were  described  as  taking  place  in  the  pleura  in  pleurisy  ; 
young  connective-tissue  formations  take  place  upon  its  sur- 
face under  the  layer  of  plastic  exudation  :  if  the  inflamma- 
tory process  is  continued  sufficiently  long,  these  are  con- 
verted into  a  firm  fibrinous  mass,  causing  either  a  permanent 
thickening  of  the  pericardium  or  else  adhesions  between 
its  two  surfaces.  Sometimes  these  adhesions  are  by  bands, 
stretching  across  from  one  portion  to  the  other,  at  other 
times  there  is  complete  agglutination  of  the  two  surfaces, 
and  an  entire  obliteration  of  the  pericardial  cavity ;  in 
either  case,  organization  more  or  less  complete  takes  place. 

In  connection  with  the  inflammatory  changes  affecting 
the  visceral  pericardium,  there  will  be  more  or  less  change 
of  an  inflammatory  nature  developed  in  the  muscular  tissue 
of  the  heart  immediately  beneath  the  pericardium.  If  the 
pericarditis  has  been  extensive  and  long-continued  the 
walls  of  the  heart  will  become  weakened,  indeed  they  are 
always  somewhat  weakened  in  every  attack  of  pericarditis. 
This  change  has  received  the  name  of  myocarditis,  and  will 
be  considered  more  fully  at  another  time.  I  will  now 
simply  state  that  dilatation  of  the  cavities  of  the  heart  may 
take  place  in  consequence  of  the  weakened  condition  of  the 
cardiac  walls,  and  cardiac  hypertrophy  may  be  developed 
as  a  result  of  this  weakening  and  dilatation.  Upon  post- 
mortem examination  not  unfrequently  white  spots  are 
found  upon  the  external  surface  of  the  heart.  As  to  the 
nature  of  these  spots,  there  has  been  considerable  discus- 


ACUTE  PERICARDITIS.  291 

sion,—  they  are,  however,  nothing  more  than  growths  of 
white  connective  tissue  immediately  beneath  the  cardiac 
pericardium,  and  indicate  the  previous  existence  of  a  local- 
ized pericardial  inflammation  which  has  been  recovered  from 
without  adhesions. 

In  rare  instances  the  two  surfaces  of  the  pericardium 
will  become  firmly  agglutinated  throughout  their  entire 
extent,  and  the  pericardial  sac  completely  obliterated. 
Under  such  circumstances  the  movements  of  the  heart 
carry  with  them  the  pericardium,  and  with  each  cardiac 
pulsation  there  is  a  lifting  of  the  diaphragm. 

I  have  already  stated  that  spots  of  ecchymosis  sometimes 
occur  in  pericarditis  in  the  early  stage  of  the  inflammatory 
process ;  they  are  also  occasionally  present  in  the  later 
stages  of  the  disease,  and  are  then  due  to  rupture  of  blood- 
vessels in  the  new  connective-tissue  formations :  when  such 
rupture  occurs,  the  serous  effusion  in  the  pericardial  sac 
will  be  blood-stained. 

ETIOLOGY. — Acute  pericarditis  rarely  occurs  as  a  primary 
affection,  but  is  usually  secondary  to  or  is  developed  during 
the  course  of  some  other  disease. 

It  may  be  produced  by  injuries  to  the  pericardium, — by  ex- 
tension of  inflammation  from  neighboring  organs,  as  when  it 
occurs  with  pneumonia,  pleurisy,  necrosis  of  the  sternum, 
ribs,  etc.  It,  however,  occurs  most  frequently  in  connection 
with  that  class  of  diseases  which  depend  upon  well-recog- 
nized blood-changes.  In  this  division  is  included  pericar- 
ditis which  accompanies  acute  rheumatism,  Bright' s  disease, 
zymotic  affections,  as  scarlatina,  small-pox,  typhus  fever, 
tuberculosis,  syphilis,  chronic  alcoholismus,  etc.  Occa- 
sionally it  is  developed  in  connection  with  scurvy  and  with 
purpura ;  then  it  is  of  the  hemorrhagic  variety.  When 
pericarditis  occurs  in  connection  with  pya3mic  and  septic 
conditions,  the  effusion  is  purulent  in  character  and  accu- 
mulates rapidly. 

It  is  of  most  frequent  occurrence  in  connection  with  acute 
articular  rheumatism  and  acute  Bright' s  disease.  Often,  in 
rheumatic  pericarditis,  the  articular  rheumatic  develop- 
ment occurs  subsequent  to  the  pericarditis ;  nevertheless  it 


292  ETIOLOGY. 

is  rheumatic  in  its  origin,  and  is  due  to  a  pre-existing  con- 
dition of  the  system  or  blood  which  favors  rheumatic  devel- 
opments. 

Pericarditis  occurring  in  connection  with  scarlet  fever  ia 
especially  liable  to  be  overlooked.  Undoubtedly,  it  very 
often  passes  unrecognized  from  the  want  of  a  careful  physical 
examination  of  the  chest,  but  in  scarlatina  a  careful  physi- 
cal examination  fails  to  detect  its  presence  until  a  large 
amount  of  fluid  effusion  takes  place.  It  may  occur  at  any 
age,  in  the  youngest  child,  and  in  very  aged  persons. 

It  rarely  if  ever  occurs  as  an  idiopathic  affection. 

SYMPTOMS. — We  now  come  to  the  consideration  of  its 
symptoms.  The  objective  symptoms  of  acute  pericarditis 
are  rarely  well  defined. 

It  is  very  difficult  to  give  a  clear  description  of  the  ra- 
tional symptoms  which  attend  its  development,  for  it  is 
usually  associated  with  some  other  affection,  the1  symptoms 
of  which  have  a  tendency  to  obscure  those  of  pericarditis  ; 
more  than  one-half  the  cases  of  pericarditis  are  latent,  and 
come  on  so  insidiously  that  they  would  go  unrecognized, 
were  it  not  for  the  physical  signs  which  attend  their  devel- 
opment. 

The  two  prominent  objective  symptoms  of  pericarditis  are 
pain  in  the  precordial  region  and  cardiac  palpitation.  The 
pain  is  usually  confined  to  the  precordial  space  ;  occasionally, 
it  involves  the  brachial  plexus,  and  extends  down  the  left 
arm :  under  such  circumstances  it  is  probably  reflex  in 
character. 

The  pain  may  be  increased  in  severity  by  pressing  the 
left  lobe  of  the  liver  against  the  diaphragm.  The  pain 
varies  in  severity ;  sometimes  it  is  very  slight,  again  it  is  of 
a  sharp  lancinating  character,  and  sufficiently  severe  to  de- 
mand immediate  relief. 

With  the  pain  there  is  always  more  or  less  cardiac  palpi- 
tation, a  dry,  irritable  cough,  and  a  sense  of  constriction 
over  the  whole  chest,  with  more  or  less  dyspnoea  ;  the  inten- 
sity of  the  dyspnoea  will  vary  with  the  amount  of  the  fluid 
effusion. 

When  the  effusion  is  considerable  the  patient  becomes  rest- 


ACUTE  PERICARDITIS.  293 

less,  and  the  countenance  assumes  an  anxious  expression, 
with  a  painful  look  of  suffering  somewhat  characteristic, 
—he  will  assume  the  half-sitting  posture,  leaning  somewhat 
toward  the  left  side, — lying  on  the  back,  with  the  head  eleva- 
ted, is  the  position  usually  preferred  by  this  class  of  patients. 

At  first,  the  pulse  is  full  and  strong,  ranging  from  90  tc 
120  beats  in  the  minute, — after  the  fluid  effusion  has  taken 
place,  it  becomes  feeble,  suppressed,  and  sometimes  delayed. 
If  the  effusion  is  abundant  the  pulse  has  a  tendency  to  be- 
come irregular,  and  not  unfrequently  intermitting, — it  is 
always  out  of  proportion  to  the  activity  of  the  heart. 

The  temperature  usually  varies  one  or  two  degrees, — in 
some  cases  it  may  rise  as  high  as  104°  F.  In  fatal  cases, 
the  temperature  falls  toward  the  close  of  life ;  it  may  fall 
below  the  normal  standard. 

Headache  and  dizziness  are  frequently  present, — in  the 
severer  forms  of  the  disease  there  is  often  delirium,  the 
patient  sometimes  becoming  so  furious  as  to  require  re- 
straint. 

Usually,  when  the  fluid  effusion  takes  place,  the  acute- 
ness  of  the  symptoms  subsides,  and  the  patient  experiences 
a  sensation  of  oppression  referable  to  the  precordium, — he 
is  disinclined  to  make  any  movement,  for  the  least  move- 
ment of  the  body  gives  rise  to  a  sinking  sensation  with  a 
tendency  to  syncope.  Under  such  circumstances  the  pa- 
tient is  constantly  in  danger  of  sudden  and  fatal  syncope 
from  pressure  of  the  pericardial  accumulation  upon  the 
heart.  It  is  maintained  by  some  that  sudden  and  fatal 
syncope  will  not  be  developed  in  primary  pericarditis,  but 
that  it  is  developed  only  after  several  attacks  have  occurred, 
and  more  or  less  extensive  pericardial  adhesions  exist  as  the 
result  of  these  attacks.  This  is  not  necessarily  the  case,  for 
whenever  large  fluid  effusions  are  developed,  with  the 
attendant  weakening  of  the  cardiac  walls,  from  superficial 
myocarditis,  patients  are  constantly  in  danger  from  sudden 
syncope.  The  severity  of  the  symptoms  in  pericarditis  cor- 
responds to  the  intensity  of  the  inflammation  and  the 
amount  of  the  effusion ;  if  the  inflammation  is  slight  and 
the  effusion  moderate,  the  plastic  exudation  predominating, 


294  SYMPTOMS. 

none  of  these  symptoms  will  be  present,  and  the  objective 
symptoms  will  only  serve  to  attract  attention  to  the  heart 
as  the  seat  of  disease. 

The  objective  symptoms  in  many  cases  of  pericarditis  be- 
ing so  obscure,  often  altogether  wanting,  the  physical  signs 
become  all-important.  In  fact,  in  all  cases  of  acute  articu- 
lar rheumatism,  for  the  first  two  weeks  it  is  your  impera- 
tive duty  each  day  to  make  a  careful  physical  examina- 
tion of  the  heart,  especially  if  the  action  of  the  heart 
becomes  irritable  and  the  apex-beat  is  increased  in  area  and 
in  force. 

The  same  care  in  examination  should  also  be  exercised  in 
acute  Bright' s  disease  of  the  kidney. 

PHYSICAL  SIGNS. — These  vary  with  the  different  stages 
of  the  disease.  In  the  early  stage  of  the  attack  the  only 
sign  furnished  by  inspection  and  palpation  is  an  irritable 
and  forcible  action  of  the  heart.  There  is  no  change  in  the 
normal  area  of  precordial  dulness  on  percussion. 

On  auscultation,  you  will  obtain  the  first  positive  physi- 
cal sign  of  the  existence  of  pericarditis,  that  is,  the  pericar- 
dial friction-sounds.  These  friction-sounds  may  be  single 
or  double,  and  they  may  accompany  or  be  independent  of 
the  heart-sounds.  They  are  always  superficial  in  charac- 
acter,  and  are  generally  restricted  to  the  precordial  space. 
Their  point  of  maximum  intensity  is  usually  at  the  junction 
of  the  fourth  rib  with  the  sternum  on  the  left  side,- — occa- 
sionally they  will  not  be  audible  at  this  point,  but  will  be 
heard  over  the  large  vessels  at  the  base  of  the  heart ;  when 
this  is  the  case  it  indicates  that  only  a  small  extent  of  the 
pericardium  is  involved,  and  that  the  inflammatory  changes 
are  confined  to  that  portion  of  the  pericardium  which  cov- 
ers the  large  vessels. 

Pericardial  friction-sounds  may  be  increased  in  intensity 
by  changing  the  position  of  the  patient  ;  when  the  body  is 
thrown  forward  the  heart  will  be  brought  nearer  to  the  an- 
terior wall  of  the  chest  and  the  friction-sound  will  be  more 
distinctly  audible.  These  friction -sounds  will  also  be  in- 
creased in  intensity  by  a  full  inspiration,  for  the  distended 
lung  will  press  the  two  pericardial  surfaces  together  and 


ACUTE  PERICARDITIS.  295 

thus  intensify  the  rubbing  sounds.  In  this  way  a  single 
friction-sound  may  become  double.  These  sounds  are  usu 
ally  of  short  duration,  disappearing  after  a  few  hours,  or  at 
most  in  a  few  days.  As  soon  as  the  stage  of  effusion  is 
reached  and  liquid  is  poured  into  the  pericardial  sac,  the 
friction-sounds  disappear  and  another  class  of  physical 
signs  are  developed  which  marks  the  effusive  stage  of  peri- 
carditis. Inspection  now  shows  a  diminution  in  the  re- 
spiratory movements  over  the  precordial  space,  and  if  the 
pericardial  sac  is  distended — especially  is  this  the  case  in 
children  and  young  persons — there  will  be  arching  forward 
of  the  precordial  region ;  this  arching  forward  may  extend 
from  the  second  to  the  sixth  intercostal  space. 

Palpation  shows  the  point  of  the  apex-beat  to  be  raised 
and  carried  to  the  left  of  its  normal  position ;  the  cardiac 
excitement  arid  friction  fremitus,  which  might  have  been 
present  before  the  effusion  occurred,  disappear,  and  if  the 
effusion  is  large  the  apex-beat  becomes  feeble  or  impercep- 
tible. Sometimes,  in  extreme  pericardial  effusion,  an  undu- 
lating impulse  is  communicated  to  the  heart  as  it  rests  on 
the  chest- walls,  by  the  action  of  the  heart  in  the  fluid. 

On  percussion,  if  considerable  effusion  has  occurred,  you 
will  find  that  the  area  of  precordial  dulness  is  increased  in 
every  direction,  especially  laterally  and  vertically.  The 
shape  of  the  enlarged  area  corresponds  to  the  pyramidal 
form  of  the  pericardial  sac.  In  a  lateral  direction  the 
precordial  dulness  may  extend  from  one  nipple  to  the 
other ;  it  may  extend  upward  as  high  as  the  second, 
and  even  as  high  as  the  first  rib ;  the  dulness  will  extend 
downward  somewhat  more  than  natural  in  the  median 
line.  The  diaphragm  may  be  somewhat  displaced  down- 
ward. 

A  small  amount  of  effusion  is  denoted  by  an  increase  in 
the  width  of  the  precordial  area  of  dulness  at  the  lower 
portion  of  the  precordial  region. 

Upon  auscultation  you  will  notice  that  there  is  an  absence 
of  the  respiratory  murmur  over  all  that  space  which  is 
normally  occupied  by  lung-tissue,  the  lung  being  pushed  to 
the  right  and  left  by  the  distended  pericardial  sac.  The 


295  PHYSICAL   SIGNS. 

friction-sound  which  was  present  before  the  occurrence  of 
the  pericardial  effusion,  is  now  absent,  and  the  heart- sounds 
become  feeble  or  are  entirely  lost ;  sometimes  the  friction- 
sound  will  continue  over  the  region  of  the  large  vessels, 
after  it  has  disappeared  at  all  other  points  over  the  pre- 
cordial  space. 

Usually,  the  effusion  does  not  remain  very  long,  its 
absorption  often  taking  place  quite  rapidly.  In  or- 
dinary cases  the  fluid  disappears  within  a  week  or  ten 
days. 

Stage  of  absorption. — As  recovery  takes  place,  and  the 
fluid  and  solid  effusion  is  absorbed,  the  bulging  of  the  pre- 
cordial  region,  which  was  present  in  the  stage  of  effusion, 
subsides,  and  the  area  of  precordial  dulness  decreases  as 
the  pericardial  surfaces  again  come  together.  These  sur- 
faces, having  become  roughened  and  thickened  by  the  in- 
flammatory process  as  they  come  together,  the  friction- 
sound  will  reappear,  the  heart-sounds  will  become  more 
distinct,  the  apex  will  assume  its  normal  position,  the 
cardiac  impulse  will  regain  its  normal  force,  and  the  respi- 
ratory and  vocal  sounds  are  again  heard  over  the  space 
formerly  occupied  by  the  distended  pericardium. 

If  the  anatomical  changes  developed  in  the  substance 
and  on  the  surface  of  the  pericardium  have  been  extensive, 
as  the  two  pericardial  surfaces  come  together  they  may 
become  firmly  adherent,  and  all  motion  between  the  heart 
and  pericardium  cease. 

This  condition  cannot  be  recognized  by  physical  examina- 
tion— it  is  only  to  be  inferred  from  the  history  of  the  case. 
If  a  person  who  has  had  all  the  symptoms  of  fluid  effusion 
into  the  pericardium,  followed  by  a  friction- sound  which 
has  gradually  disappeared,  leaving  a  slight  intermittent 
action  of  the  heart,  suffers  on  active  exertion  from  a  sense 
of  constriction  about  the  precordial  region,  it  may  be  in- 
ferred that  adhesions  between  the  two  surfaces  of  the  peri- 
cardium have  taken  place. 

Pericardial  adhesions,  whether  general  or  by  means  of 
bands,  as  already  described,  may  subsequently  undergo 
absorption,  and  if  a  second  attack  of  pericarditis  is  never 


ACUTE   PEEICAEDITIS.  297 

developed,  after  a  long  time  the  motion  between  the  two 
surfaces  is  entirely  restored,  and  no  signs  will  be  left  to 
indicate  that  the  patient  has  ever  suffered  from  the  affec- 
tion, except  the  presence  of  white  spots  upon  the  peri- 
cardium, which  may  be  visible  at  the  post-mortem  exami 
nation. 


LECTURE  XXV. 


ACUTE  PERICARDITIS. 


Chrome  Pericarditis. — Hydropericardium. — Pneumopericardium. — Hsemope- 
ricardiuru. — Tubercles  of  the  Pericardium. 


I  SHALL  this  morning  continue  the  subject  of  acute  pericar- 
ditis by  inviting  your  attention  to  some  points  in  connection 
with  its  differential  diagnosis. 

DIFFERENTIAL  DIAGNOSIS. — The  existence  of  pericarditis 
can  never  be  positively  determined  except  by  the  physical 
signs  which  may  attend  its  development  ;  even  when  your 
attention  has  been  directed  to  the  heart,  it  is  not  always 
easy  to  recognize  its  presence.  The  physical  signs  of  peri- 
carditis may  be  confounded  with  those  of  endocarditis, 
pleurisy,  and  cardiac  hypertrophy. 

The  friction-murmurs  of  pericarditis  may  be  distinguished 
from  endocardial  murmurs  : — First,  by  their  superficial  char- 
acter. Second,  by  the  area  of  their  diffusion,  being  usually 
confined  to  the  precordial  space,  and  having  their  maximum 
intensity  over  the  right  ventricle  on  the  left  side,  at  the 
junction  of  the  fourth  rib  with  the  sternum  ;  while  endocar- 
dial murmurs  are  audible  beyond  the  limits  of  the  heart  to 
the  right  and  left,  and  upward  along  the  course  of  the  ves- 
sels. TJiird,  the  intensity  of  a  pericardial  friction-sound 
may  be  increased  or  diminished,  by  inclining  the  body  oi 
the  patient  backward  or  forward,  and  it  is  rendered  more 
distinct  by  a  full  inspiration ;  whereas,  endocardial  mur- 
murs are  not  changed  in  intensity  by  a  change  in  the  posi 
tion  of  the  patient,  nor  by  the  period  nor  the  time  of  the 


ACUTE   PEEICAEDITIS.  29£ 

respiratory  movement.  Fourth*  pericardial  friction-sounds 
are  not  necessarily  synchronous  with  the  heart-sounds  ; 
while  endocardial  murmurs  are  always  connected  with  them, 
either  preceding,  taking  the  place  of,  or  immediately  follow- 
ing them.  By  careful  observation  you  will  always  be  able 
to  make  a  differential  diagnosis  between  endocardial  and 
pericardial  murmurs. 

Pericardial  friction-sounds  may  be  distinguished  from  the 
friction- sounds  of  pleurisy,  when  the  pleurisy  occurs  over 
the  precordial  space,  by  directing  the  patient  to  hold  his 
breath  for  a  moment ;  if  the  friction-sound  is  pericardial  it 
will  continue  during  the  suspension  of  the  respiratory  act, 
—if  it  is  pleuritic,  the  friction-sound  will  cease  during  the 
arrest  of  the  respiration.  Occasionally  however,  where  there 
is  consolidation  of  the  lung  directly  over  the  heart,  accompa- 
nied by  a  pleuritic  friction,  and  firm  adhesions  have  taken 
place  between  the  two  surfaces  of  the  pericardium,  a  dis- 
tinct friction-sound  may  be  produced  in  the  pleura  by  the 
motion  of  the  heart  in  the  chest-cavity.  This  is  of  rare  oc- 
currence, and  is  hardly  to  be  taken  into  consideration. 

The  abnormal  area  of  percussion  dulness  produced  by 
hypertrophy,  or  dilatation  of  the  right  ventricle,  very 
closely  resembles  that  produced  by  pericardial  effusion,  and 
it  is  often  exceedingly  difficult  to  draw  a  distinct  line  of 
differential  diagnosis.  There  is  one  point  which  may  be  re- 
garded as  almost  diagnostic  ;  and  that  is,  in  enlargement  of 
the  right  heart  the  dulness  never  extends  to  the  left  beyond 
the  apex-beat,  while  in  pericardial  effusion  the  dulness 
may  extend  perhaps  one  or  two  inches  beyond  the  apex- 
beat.  The  fact  that  cardiac  dulness  extends  beyond  the 
apex-beat  to  the  right  as  well  as  the  left,  proves  that  there 
is  more  or  less  fluid  in  the  pericardial  sac.  Besides,  the  ex- 
istence of  cardiac  hypertrophy  is  determined  by  an  increase 
in  the  force  of  the  apex-beat,  and  the  greater  than  normal 
intensity  of  the  heart-sounds  ;  while  in  pericarditis  with 
effusion,  both  will  be  diminished  in  intensity.  Pericardial 
effusion  is  distinguished  from  hypertrophy,  or  dilatation  of 
the  left  heart,  by  the  fact  that  in  left  cardiac  hypertrophy 
the  apex-beat  is  carried  downward  and  to  the  left,  and  the 


300  PROGNOSIS. 

area  of  precordial  dulness  is  increased  in  the  same  direction, 
and  not  to  the  right ;  also,  the  force  of  the  heart's  action  is 
very  greatly  increased  in  hypertrophy. 

PROGNOSIS. — In  most  instances  pericarditis  ends  in  com- 
plete recovery  ;  the  exceptions  to  this  rule  are  met  with 
almost  exclusively  in  connection  with  Bright' s  disease  of 
the  kidney,  and  septic  or  pyaemic  "conditions.  In  connec- 
tion with  either  of  these  diseases,  there  is  always  more  or 
less  danger  ;  if  it  occurs  in  connection  with  pyaemia  there  is 
very  great  danger,  for  the  reason  that  the  exudation  which 
occurs  in  these  cases  is  usually  purulent  in  character,  and 
its  absorption  can  hardly  be  hoped  for,  although  occasion- 
ally it  does  occur.  The  nature  of  the  exudation  determines 
to  a  great  extent  the  prognosis  ;  when  it  is  hemorrhagic  or 
purulent,  the  prognosis  is  bad. 

Occasionally,  acute  pericarditis  passes  into  chronic,  or 
rather  is  accompanied  by  a  large  serous  effusion,  which 
disappears  slowly,  and  is  especially  liable  to  be  accompanied 
by  relapses,  and  thus  the  disease  goes  on  for  months. 
During  the  progress  of  the  disease,  sometimes  the  patient 
suffers  from  attacks  of  extreme  dyspnoea  ;  in  rare  instances 
a  fatal  syncope  occurs. 

As  a  result  of  the  long  continuance  of  the  fluid  effusion, 
the  substance  of  the  heart  becomes  softened,  and  more  or 
less  degeneration  of  the  muscular  tissue  of  the  heart  occurs, 
on  account  of  which  the  organ  is  enfeebled,  its  propelling 
power  is  diminished,  and  death  by  oedema  of  the  lungs  may 
occur.  This  form  of  subacute  or  chronic  pericarditis  is 
generally  associated  with  blood-changes,  attended  by  a 
loss  of  red  globules  and  fibrin,  and  must  always  be  regarded 
as  a  grave  form  of  disease.  Pericarditis,  which  accom- 
panies acute  rheumatism,  is  rarely  ever  fatal.  The  most 
frequent  sequelae  of  this  form  of  pericarditis  are  adhesions 
of  the  two  surfaces  of  the  pericardium,  cardiac  dilatation, 
and  hypertrophy  ;  all  of  which  are  more  likely  to  develop, 
the  longer  the  duration  of  the  attack. 

The  cardiac  dilatation  occurs  as  the  result  of  the  weaken- 
ing of  the  cardiac  walls  from  the  inflammatory  process  going 
on  incidentally  underneath  the  endocardium ;  and  the  hyper- 


ACUTE   PERICARDITIS.  301 

trophy  of  the  cardiac  walls  which  follows  the  dilatation  is 
compensatory. 

There  is  still  another  interesting  fact  affecting  the  progno- 
sis in  pericarditis,  taking  into  consideration  its  sequelae,  and 
that  is,  occasionally  the  pericardial  exudation  is  abundant, 
and  extensive  pericardial  adhesions  take  place  at  the  base 
of  the  heart,  which,  by  their  contraction  and  pressure, 
interfere  with  the  current  of  blood  through  the  coronary 
arteries,  and  as  a  result  of  this  interference  with  nutrition 
of  the  heart,  fatty  degeneration  of  its  walls  may  be  devel- 
oped. This  is  not  of  very  frequent  occurrence  ;  occasionally 
it  is  met  with,  and  it  should  be  remembered  as  one  of  the 
causes  of  fatty  degeneration  of  the  heart. 

We  now  come  to  the  treatment  of  this  affection,  which  I 
shall  consider  somewhat  briefly,  as  it  will  be  necessary  to 
refer  to  it  again  under  the  head  of  the  general  management 
of  cardiac  diseases. 

TREATMENT. — At  the  present  time,  it  is  difficult  to  lay 
down  a  plan  of  treatment  in  pericarditis  which  shall  re- 
ceive the  full  sanction  of  the  profession. 

Although  we  have  to  deal  with  an  inflammation  of  con- 
siderable severity,  yet  with  our  present  views  of  the  eti- 
ology and  morbid  anatomy  of  the  disease  we  are  not  war- 
ranted in  the  use  of  a  single  so-called  antiphlogistic  meas- 
ure. Blood-letting,  hydragogue  cathartics,  diuretics,  and 
blisters,  which  at  one  time  were  almost  universally  -em- 
ployed, are  gradually  being  abandoned  ;  the  tendency  of 
the  profession  is  towards  a  supporting  plan  of  treatment. 

When  it  is  determined  that  pericarditis  exists,  first  en- 
deavor to  seek  out  its  cause  ;  for,  as  I  have  already  stated, 
it  is  rarely  if  ever  a  primary  disease.  When  the  cause  is 
found,  if  possible  remove  it, — if  this  is  impossible,  coun- 
teract it  as  far  as  you  are  able. 

If  the  pericarditis  is  due  to  an  excess  of  urea  in  the  cir- 
culation, at  once  adopt  measures  for  its  removal.  What 
these  measures  are  which  may  be  employed,  will  be  defi- 
nitely referred  to  in  another  connection. 

If  it  depends  upon  articular  rheumatism,  those  remedies 
which  have,  or  are  supposed  to  have,  the  power  of  changing 


COLLIE  12 IE   01- 


302  TREATMENT. 

the  morbid  condition  of  the  blood,  upon  which  the  rheu- 
matic developments  depend,  must  be  administered. 

In  those  forms  of  fever  which  are  marked  by  great  depres- 
sion, the  occurrence  of  pericarditis  indicates  an  increase 
in  the  quantity  of  stimulants  already  being  administered. 
Under  all  such  circumstances,  especially  in  connection  with 
septic  and  pysemic  developments,  supporting  measures  are 
called  for.  At  the  present  time,  in  the  early  stage  of  peri- 
carditis, the  most  favorite  local  application  is  hot  anodyne 
poultices  over  the  precordial  space. 

The  relief  afforded  to  a  patient  suffering  from  pericarditis 
from  these  applications  is  sometimes  remarkable  ;  they  not 
only  relieve  pain,  but  apparently  arrest  the  progress  of  the 
inflammatory  action. 

The  most  valuable  internal  remedial  agent  in  the  early 
stage  of  this  disease  is  opium.  It  should  never  be  given  in 
large  doses,  but  only  in  sufficient  quantity  to  relieve  pain 
and  arrest  or  allay  the  irritable  action  of  the  heart.  The 
largest  doses  administered  should  be  given  at  night,  in  order 
that  the  patient  may  secure  quiet  sleep  ;  the  heart  is  more 
liable  to  become  irritable  at  night,  and  the  patient  usually 
becomes  more  restless.  Great  care  should  be  exercised  in 
the  administration  of  opium  ;  it  should  never  be  carried  to 
narcotism,  for  the  effect  would  be  to  diminish  the  force  of 
the  heart'  s  action,  which  is  not  desirable. 

In  the  stage  of  effusion,  if  the  liquid  within  the  pericar- 
dium is  sufficient  in  quantity  to  enfeeble  the  heart  by  com- 
pression, it  must  be  removed  as  quickly  as  possible  ;  and  the 
question  arises,  what  are  the  means  to  be  relied  upon  for  ac- 
plishing  this  result  ?  So  long  as  you  are  able  to  steady  and 
sustain  your  patient  under  the  depressing  symptoms  which 
usually  attend  the  commencement  of  the  effusive  stage,  and 
there  are  no  evidences  that  pulmonary  congestion  and 
oedema  are  occurring  as  the  result  of  the  enfeebled  heart's 
action,  immediate  interference  may  be  delayed  ;  and  per- 
haps, after  a  few  hours  have  elapsed,  the  apparently  danger.- 
ous  period  will  have  been  passed,  and  a  rapid  disappear- 
ance of  the  fluid  will  take  place. 

As  I  have  already  stated,  the  means  which  have  been 


riFj 


ACUTE  PERICAEDITIS.  303 

usually  employed  to  accomplish  the  removal  of  the  fluid, 
are  hydragogue  cathartics,  diuretics,  and  blisters.  I  am 
convinced  that  this  plan  of  treatment  will  not  hasten,  but 
rather  delay  the  removal  of  the  fluid.  Experience  teaches 
that  pericarditis  is  an  inflammation  which  occurs  in  the 
weak  and  feeble,  and  not  in  the  strong  and  vigorous, — is  met 
with  among  the  young  rather  than  in  healthy  persons  in  the 
prime  of  life.  In  almost  all  instances,  it  is  associated  with 
those  diseases  that  are  especially  marked  by  a  loss  of 
vitality  ;  consequently  all  measures  which  have  a  tendency 
to  depress  the  patient  are  to  be  avoided. 

The  same  arguments  which  were  used  in  regard  to  the 
proper  means  to  be  employed  for  promoting  the  absorption 
of  the  fluid  in  pleurisy,  may  be  applied  with  equal  force  to 
the  treatment  of  pericarditis.  In  both  instances  there  can 
be  no  question  but  that  the  removal  of  the  fluid  and  plastic 
effusions  go  on  most  rapidly  when  the  nutritive  processes 
are  most  active.  Therefore,  the  same  general  rules  which 
were  given  to  guide  you  in  promoting  the  absorption  of  the 
inflammatory  product  in  pleurisy,  are  to  be  followed  in  the 
treatment  of  pericarditis.  Iron  and  stimulants  will  be 
equally  of  service  in  pericarditis  as  in  pleurisy.  In  the 
treatment  of  pericarditis,  you  must  bear  in  mind  that  any- 
thing which  accelerates  the  heart's  action  should  be  care- 
fully avoided. 

A  patient  with  pericarditis  should  not  be  allowed  to  get 
out  of  bed,  and  from  the  very  commencement  of  the  at- 
tack he  should  be  kept  absolutely  quiet.  He  must  be 
removed  from  all  those  surroundings  which  cause  excite- 
ment ;  absolute  rest  in  the  recumbent  posture  must  be  in- 
sisted upon,  and  the  surface  of  the  chest  must  be  carefully 
protected  from  the  influences  of  change  in  temperature. 
The  exposure  incident  to  a  physical  examination  of  the 
chest  will  do  the  patient  harm  unless  carefully  performed. 
Keep  the  chest  well  covered  with  flannel,  and  when  you 
make  your  physical  examination,  only  remove  the  covering 
sufficiently  to  apply  the  chest-piece  of  the  stethoscope  to 
the  surface  of  the  part  to  be  examined. 

Some  authorities  speak  very  favorably  of  the  effect  of 


304  TREATMENT. 

digitalis  as  a  controller  of  the  action  of  the  heart  in  the 
acute  stage  of  pericarditis  ;  they  say  that  it  not  only  moder- 
ates the  force  of  the  heart's  action,  but  diminishes  its  fre- 
quency. It  may  diminish  its  frequency,  but  never  its  force  ; 
while  opium  accomplishes  both  results  far  better  than  the 
digitalis.  Opium,  iron,  moderate  stimulation,  rest  in  the 
recumbent  posture,  anodyne  poultices,  and  concentrated 
nutrition,  are  about  the  only  measures  which  I  have  found 
of  service  in  the  treatment  of  acute  pericarditis. 

During  the  period  of  convalescence,  the  patient  must  be 
very  strictly  guarded,  for  the  walls  of  the  heart  are  in  a 
weakened  condition  ;  and  whenever  the  heart  is  overtaxed, 
its  cavities  are  liable  to  become  dilated,  and  cardiac  hyper- 
trophy may  be  developed  as  the  result.  Whenever  cardiac 
hypertrophy  is  once  developed,  its  tendency  is  to  progress. 
Everything  which  will  have  a  tendency  to  increase  the  ac- 
tion of  the  heart  must  be  carefully  avoided.  Children 
should  not  be  allowed  to  go  up  and  down  stairs,  or  to  play 
with  other  children  during  the  period  of  convalescence. 

Patients  convalescing  from  pericarditis  must  be  placed 
under  the  very  best  hygienic  conditions  for  two  or  three 
months  after  the  disappearance  of  the  pericardial  symp- 
toms. 

I  wish  to  say  a  few  words  concerning  aspiration.  Some- 
times, as  I  have  already  stated,  the  symptoms  which  attend 
a  large  fluid  effusion  become  very  urgent,  and  the  question 
presents  itself,  shall  aspiration  of  the  pericardium  be  per- 
formed ?  This  operation  has  been  performed,  and  it  has  been 
claimed  that  little  danger  attends  it ;  but  it  should  never  be 
rashly  undertaken.  If  it  can  be  positively  determined  that 
pus  is  present  in  the  pericardium,  you  need  not  hesitate, 
but  resort  to  aspiration  for  its  removal.  When  the  effusion 
is  sero-fibrinous,  it  must  be  remembered  that  the  urgent 
symptoms,  for  the  relief  of  which  aspiration  would  be  re- 
sorted to,  are  usually  of  short  duration,  and  patients  rarely 
die  from  the  pressure  produced  by  the  effusion:  Whether 
aspiration  shall  be  performed  under  such  circumstances, 
is  a  question  for  most  careful  consideration.  Before  leav- 
ing this  subject,  I  will  say  a  few  words  concerning  what 


ACUTE  PERICARDITIS.  30."; 

has  been  termed  chronic  pericarditis,  which  is  a  rare  form 
of  disease. 

The  adhesions  which  form  in  acute  pericarditis  cannot  be 
regarded  as  constituting  a  chronic  form  of  pericarditis. 
Generally  when  adhesions  have  taken  place,  the  inflamma- 
tion is  at  an  end,  and  this  may  occur  during  the  first  three 
or  four  weeks  of  the  disease. 

CHRONIC  PERICARDITIS. — This  may  follow  as  the  result 
of  the  acute  form,  or  it  may  be  subacute  from  its  com- 
mencement. When,  after  three  or  four  weeks,  acute  peri- 
carditis does  not  terminate  in  recovery,  it  becomes  chronic. 
In  some  cases  of  chronic  pericarditis  the  pericardial  sac 
contains  fluid,  in  other  cases  firm  adhesions  form  between 
the  pericardial  surfaces,  binding  them  more  or  less  closely 
to  each  other  ;  mingled  with  these  adhesions  are  chalky  de- 
bris and  calcareous  plates.  The  processes  which  attend 
these  anatomical  changes  have  already  been  considered. 
The  symptoms  of  chronic  pericarditis  are  those  which  give 
evidence  of  obstructed  circulation  with  signs  of  enlarge- 
ment of  the  heart, — there  is  dyspnoea,  uneasiness  or  sense 
of  weight  in  the  precordial  region.  In  some  instances,  this 
condition  is  associated  with  attacks  of  angina  pectoris. 
The  heart's  action  is  easily  disturbed,  and  cardiac  palpi- 
tation is  present  on  slight  physical  exertion  or  mental  ex- 
citement. 

The  physical  signs  of  chronic  pericarditis  closely  resem- 
ble those  of  eccentric  cardiac  hypertrophy  ;  in  both  cases, 
there  is  increased  dulness  in  the  precordial  region,  but  in 
pericarditis  the  apex-beat  is  indistinct  and  is  raised  above 
its  normal  position,  while  in  hypertrophy  the  apex-beat  is 
distinct  and  is  carried  downward  and  to  the  left  of  its  nor- 
mal position. 

If  the  two  surfaces  of  the  pericardium  are  closely  agglu- 
tinated, and  the  pericardium  is  adherent  to  the  costal  pleura, 
so  that  firm  adhesions  are  formed  between  it  and  the  chest- 
wall,  there  will  be  more  or  less  depression  of  the  precordial 
region  ;  the  cardiac  impulse  will  be  permanently  displaced 
upwards,  and  will  be  unaltered  either  by  change  of  posture, 
or  by  a  full  inspiration,  and  there  will  be  an  irregular  jog- 
so 


306  ETIOLOGY. 

ging;  motion  of  the  heart  during  both  its  systole  and  dias- 
tole. 

/Although  the  diagnosis  of  chronic  pericarditis  is  always 
difficult,  and  its  existence  rarely  if  ever  positively  deter- 
mined, unless  there  is  a  large  amount  of  fluid  effusion  in 
the  pericardial  sac  ;  still,  if  the  symptoms  and  physical 
signs  already  detailed  follow  an  attack  of  acute  pericarditis, 
there  is  presumptive  evidence  of  its  existence. 

The  prognosis  in  this  affection,  as  regards  complete  recov- 
ery, is  always  doubtful,  and  when  it  accompanies  degenera- 
tion of  the  cardiac  walls  and  valvular  insufficiency,  no  very 
great  prolongation  of  life  can  be  hoped  for. 

The  treatment  consists  in  limiting  physical  exercise,  so  as 
not  to  overtax  the  embarrassed  heart  ;  at  the  same  time  to 
furnish  the  patient  with  a  most  nutritious,  but  non-stimulat- 
ing diet,  and  to  administer  daily  some  preparation  of  iron. 

In  connection  with  inflammatory  effusions  in  the  pericar- 
dium, it  is  necessary  to  call  your  attention  for  a  few  moments 
to  a  non-inflammatory  pericardial  effusion,  which  is  called 
hydropericardium. 

HYDROPERICARDIUM  is  a  sero-albuminous  effusion  into  the 
pericardial  sac,  non-inflammatory  in  character,  and  when 
absorbed  leaves  no  trace  behind  it.  It  is  often  very  abun- 
dant, and  a  source  of  great  discomfort  to  the  patient,  but 
rarely  directly  causes  death. 

The  effect  of  such  fluid  effusions  is  to  embarrass  the  action 
of  the  heart,  while  the  heart-fibre  becomes  pale  and  is  easily 
torn,  the  result  of  the  serous  infiltration. 

ETIOLOGY. — Non-inflammatory  effusions  into  the  pericar- 
dium occur  most  frequently  in  connection  with  renal  and 
cardiac  diseases.  In  that  form  of  renal  disease  which  com- 
plicates scarlatina,  it  is  especially  liable  to  occur,  and  under 
such  circumstances  it  is  entirely  passive  in  character,  and 
is  soon  reabsorbed  on  the  return  of  the  renal  function. 
When  it  occurs  in  chronic  forms  of  Bright' s  disease,  it  is 
more  serious  and  obstinate  in  character.  When  it  occurs  in 
connection  with  chronic  cardiac  disease,  it  is  the  result  of 
the  general  venous  congestion,  and  its  pressure  greatly  em- 
barrasses the  already  enfeebled  heart. 


HYDROPERICARDIUM.  307 

It  may  occur  in  connection  with  general  dropsy  from 
any  cause.  The  general  symptoms  and  the  physical  signs 
which  attend  such  effusions  do  not  materially  differ  from 
those  already  detailed  as  marking  the  stage  of  fluid  effu- 
sion in  pericarditis,  except  that  there  is  entire  absence  of 
any  febrile  disturbance.  There  is  no  friction -sound  present 
at  any  time  during  the  progress  of  the  effusion. 

PROGNOSIS. — In  chronic  Bright' s  disease,  and  in  advanced 
cardiac  disease,  it  is  usually  the  precursor,  although  it  can 
scarcely  be  called  the  cause  of  death.  In  other  conditions, 
the  prognosis  will  depend  upon  the  circumstances  which 
attend  its  development. 

TREATMENT. — In  the  treatment  we  must  be  guided  by  the 
peculiarities  of  each  case.  All  the  measures  recommended 
for  the  treatment  of  hydrothorax  may  be  employed  in  the 
treatment  of  hydropericardium.  To  find  out  and  remove 
its  cause  is  of  the  greatest  importance  ;  in  other  words,  treat 
the  diseased  condition  which  gives  rise  to,  or  permits  the 
effusion. 

PNEUMOPERICARDIUM,  or  air  in  the  pericardial  sac,  is  the 
result  either  of  a  perforating  wound  of  the  thorax,  or  the 
perforation  of  the  pericardial  sac  by  an  ulcerative  process 
and  the  admission  of  air  from  some  organ  which  naturally 
contains  air. 

The  diagnosis  of  this  accident  rests  on  the  tympanitic 
percussion-sound  over  the  precordial  space,  and  the  tink- 
ling or  splashing  sound  heard  directly  over  the  heart. 

With  the  exception  of  those  cases  which  are  of  traumatic 
origin,  this  accident  rapidly  proves  fatal. 

Its  treatment  is  altogether  symptomatic. 

ELEMOPERICARDIUM,  or  blood  in  the  pericardial  sac,  may 
be  of  traumatic  origin,  or  may  result  from  rupture  of  the 
cardiac  walls,  or,  far  more  frequently,  the  pericardium  be- 
comes distended  with  blood  from  the  rupture  of  one  of  those 
small  aortic  aneurisms  which  develop  on  that  portion  of  the 
aorta  included  within  the  pericardial  sac.  Unless  of  trau- 
matic origin,  it  rapidly  proves  fatal,  and  will  be  found  at  the 
autopsy  of  many  cases  of  sudden  death.  When  of  trau- 
matic origin,  the  effused  blood  not  unfrequently  is  absorbed. 


308  TUBERCULOSIS   OF   PERICARDIUM. 

Tuberculosis  of  ifie  pericardium  is  only  met  with  in  con- 
nection with  acute  general  miliary  tuberculosis.  Unless 
the  tubercular  development  takes  place  only  a  short  time 
previous  to  death,  it  will  give  rise  to  pericarditis.  Its  pres- 
ence may  be  suspected  from  the  fact  of  the  pericarditis  in 
connection  with  the  symptoms  of  the  general  tuberculosis. 

The  pericardium  may  be  the  seat  of  cancer,  but  the  can- 
cerous development  is  always  secondary  to  cancerous  devel- 
opments in  other  parts  of  the  body. 


LECTURE    XXVI. 


ENDOCARDITIS. 


Acute  Endocarditis. — Ulcerative  Endocarditis. 

I  SHALL  this  morning  pass  from  inflammations  of  the 
serous  membrane  investing  the  heart,  to  inflammations  of 
the  membrane  lining  its  cavities. 

In  doing  this,  I  do  not  claim  that  the  endocardium  is  a 
serous  membrane,  but  I  do  claim  that  when  it  is  inflamed  it 
acts  in  all  respects  like  a  serous  membrane.  This  mem- 
brane not  only  lines  the  cavities  and  covers  the  valves  of 
the  heart,  but  it  is  continuous  with  the  lining  membrane  of 
the  blood-vessels  throughout  the  entire  vascular  system  ; 
any  portion  of  it  may  be  the  seat  of  inflammation,  but  that 
portion  covering  the  valves  is  especially  liable  to  take  on 
inflammation,  which  may  extend  and  involve  the  whole 
endocardial  surface  of  a  ventricle  or  an  auricle. 

I  shall  describe  two  forms  of  endocarditis,  acute  and 
chronic,  although  it  may  be  difficult  and  often  impossible 
to  draw  the  line  of  demarcation  between  them,  for  acute  runs 
into  chronic  by  a  gradual  process,  having  no  well-defined 
line  of  separation ;  still,  those  changes  which  occur  within 
the  first  few  weeks  after  the  commencement  of  the  attack 
may  properly  be  called  acute,  and  those  that  come  on  grad- 
ually several  weeks  or  months  after  the  commencement  of 
the  endocardial  inflammation,  may  properly  be  classed  as 
chronic. 

I  shall  first  describe  the  anatomical  changes  of  the  acute 
form. 


310  MORBID   ANATOMY. 

Acute  endocarditis  occurring  in  adults  usually  has  its 
seat  in  the  left  heart,  while  in  intra-uterine  life  it  occurs 
almost  exclusively  in  the  right  heart. 

MOKBID  ANATOMY. — The  first  textural  change  that  takes 
place  in  that  portion  of  the  endocardium  which  is  the 
seat  of  the  inflammatory  action,  is  a  reddening  of  the  mem- 
brane from  a  punctate  or  arborescent  vascularity.  Care 
must  be  taken  not  to  confound  this  redness  with  mere  post- 
mortem staining  of  the  membrane,  which  is  of  quite  fre- 
quent occurrence.  This  congestion  is  followed  by  opacity 
and  thickening  of  the  endocardium,  especially  on  the  free 
surface  of  the  valves,  causing  the  valves  to  present  a 
swollen  appearance,  and  to  have  an  elastic  feel ;  the  swell- 
ing is  due  to  serous  infiltration  beneath,  and  in  the  sub- 
stance of  the  endocardium.  The  serous  infiltration  is  ac- 
companied by  the  accumulation  of  a  large  number  of  young 
cells  in  the  substance  of  the  membrane,  which  causes  little 
villi  or  granulations  to  project  upon  its  free  surface.  If  the 
inflammatory  stimulant  is  continued,  the  cell  formations  go 
on  until  they  cause  warty  prominences  on  the  surface  of 
the  valve ;  on  these  projections  fibrin  from  the  blood  as  it 
passes  through  the  cavities  of  the  heart  may  be  deposited, 
so  as  to  form  fibrinous  vegetations  of  considerable  size. 
These  little  elevations  act  in  the  same  manner  as  a  foreign 
body  in  the  circulation,  and  thus  cause  the  deposit  of 
fibrin  on  their  surface.  There  is  no  other  change  on 
the  free  surface  of  the  endocardium,  except  the  loss  of  its 
endothelium.  The  free  edges  of  the  valves  are  always 
more  or  less  thickened,  and  the  fibrinous  vegetations  are 
chiefly  deposited  on  the  surface  which  is  opposed  to  the 
current  of  the  circulation. 

Sometimes  the  cell  formation  in  the  substance  and  under- 
neath the  endocardium  is  so  rapid  that  minute  abscesses 
are  formed,  the  endocardium  containing  or  covering  these 
abscesses  ruptures,  and  their  contents  are  carried  away  in 
the  current  of  the  circulation,  while  at  the  point  of  rupture 
changes  take  place  which  cause  the  endocardium  to  pre- 
sent the  appearance  of  an  ulcer. 

Again,  these  little  elevations  which  have  been  capped 


ACUTE  ENDOCARDITIS.  311 

with  fibrin  taken  from  the  blood,  may  undergo  degenera- 
tion, and  be  swept  away  in  the  current  of  the  circulation 
With  them  are  carried  portions  of  the  endocardium,  which 
from  loss  of  substance  also  presents  the  appearance  of  an 
ulcer.  These  ulcers,  thus  established,  sometimes  penetrate 
through  the  substance  of  the  valves  and  cause  perforations  ; 
this  is  one  of  the  most  dangerous  accidents  of  acute  endo- 
carditis. 

The  same  thickening,  effusion,  increase  of  cells,  and  ulcer- 
ations  may  take  place  in  any  portion  of  the  endocardium. 
If  the  effusion  takes  place  on  its  free  auricular  or  ventricu- 
lar surface,  the  major  portion  of  it  will  be  washed  away  by 
the  current  of  the  circulation,  and  thickening  of  the  endo- 
cardium at  the  point  where  the  exudation  occurred  will  be 
the  only  appreciable  change. 

Endocardial  inflammation  is  usually  accompanied  by 
more  or  less  inflammation  of  the  muscular  structure  under- 
neath ;  this  myocarditis  may  extend  some  depth  into  the 
muscular  structure,  and  by  weakening  it  and  altering  its 
consistency  lead  to  bulging  and  the  formation  of  a  ventricu- 
lar aneurism.  Rupture  of  one  or  more  of  the  chordae  ten- 
dinese  sometimes  occurs  in  acute  endocarditis,  as  the  result 
of  the  ulcerative  processes  already  described.  Occasion- 
ally, some  of  the  fibrinous  deposits  upon  the  free  surface 
of  the  valves,  after  being  detached,  enter  the  circulation 
and  give  rise  to  embolism  in  the  brain  or  some  other 
organ ;  or  some  of  the  inflammatory  products  already  re- 
ferred to  may  be  carried  into  the  circulation  and  produce 
septicsemia. 

If  the  inflammatory  processes  subside,  the  young  connec- 
tive-tissue formations  develop  into  fibrous  structure  and 
lead  to  permanent  organic  changes,  which  will  be  considered 
under  the  head  of  chronic  endocarditis. 

ETIOLOGY. — Acute  endocarditis  rarely  if  ever  occurs  as  a 
primary  affection ;  it  is  most  frequently  met  with  in  the 
course  of  those  affections  which  depend  upon,  or  are  at- 
tended by  morbid  changes  in  the  blood.  These  changes 
cause  the  blood  to  become  more  or  less  irritating  to  the  free 
surface  of  the  endocardium  over  which  it  passes  ;  what  the 


312  ETIOLOGY. 

exact  nature  of  the  irritating  element  may  be,  cannot  be 
determined  in  every  instance.  It  occurs  frequently  in  con- 
nection with  Bright' s  disease  of  the  kidney,  and  then  is 
probably  due  to  the  irritation  produced  by  the  excess  of 
urea  in  the  circulation.  In  the  majority  of  instances,  acute 
endocarditis  is  developed  during  an  attack  of  acute  articu- 
lar rheumatism ;  yet,  a  large  number  of  cases  of  acute 
rheumatism  run  their  course  without  any  endocardial  in- 
flammation. When  it  occurs  in  a  rheumatic  patient,  whether 
it  is  due  to  the  change  in  the  salts  of  the  blood,  or  to  a  dis- 
tinct poison  which  may  be  designated  as  the  rheumatic 
poison,  which  acts  as  an  irritant  to  the  valvular  surface  of 
the  endocardium,  has  not  been  definitely  determined. 

I  formerly  taught  that  the  fibrous  framework  of  the 
valves  was  the  primary  seat  of  the  inflammatory  action  in 
endocarditis,  and  that  from  this  point  the  inflammation  ex- 
tended to  other  portions  of  the  endocardium.  A  more  care- 
ful analysis  of  the  anatomical  changes  in  endocarditis  has 
convinced  me  that  the  primary  seat  of  the  inflammatory 
changes  is  in  the  serous  structure,  and  that  the  changes 
which  occur  in  the  fibrous  framework  of  the  valves  are  sec- 
ondary ;  also,  that  in  the  majority  of  instances  the  inflam- 
mation is  excited  by  the  action  of  a  direct  irritant  upon  the 
surface  of  the  endocardium.  The  valves  being  the  most 
prominent  points  within  the  heart,  are  the  most  exposed  to 
the  irritating  influence  of  the  changed  blood,  and  conse- 
quently the  endocardium  covering  them  is  the  primary  seat 
of  the  inflammatory  process.  This  seems  to  me  by  far 
the  most  reasonable  hypothesis  yet  advanced. 

It  has  been  claimed  that  endocarditis  may  occur  as  the 
result  of  an  extension  of  pericardial  inflammation  to  the 
inner  surface  of  the  vessels  at  the  base  of  the  heart ;  this 
may  be  possible  but  not  probable.  There  is  no  disease 
which  depends  upon,  or  gives  rise  to  morbid  condition  of 
the  blood,  with  which  endocarditis  may  not  occur  as  a  com- 
plication. Hence,  its  frequent  ocurrence  in  the  essential 
and  exanthematous  fevers  ;  in  diphtheria,  septicaemia,  pyae- 
mia, etc.  ;  the  result,  in  all  such  instances,  of  the  direct  ir- 
ritation of  the  endocardium  by  the  poisoned  blood. 


ACUTE  E1STDOCAEDITIS.  313 

SYMPTOMS. — Without  the  physical  signs,  perhaps  there  is 
no  disease  more  obscure  than  acute  endocarditis.  It  often 
runs  its  entire  course  without  giving  any  evidence  of  its 
existence,  except  such  as  is  furnished  by  auscultation. 
The  objective  symptoms  are  even  less  distinct  than  those  ot 
pericarditis.  There  is  scarcely  anything  to  direct  your  at- 
tention to  the  heart,  and  you  are  liable  to  have  your  atten- 
tion absorbed  by  the  general  progress  of  the  disease  which 
the  endocarditis  may  complicate.  In  a  large  majority  of 
cases  of  endocarditis  complicating  articular  rheumatism, 
the  attention  of  the  patient  as  well  as  that  of  the  physician 
is  fully  occupied  with  the  painful  joint  affection.  If,  how- 
ever, the  endocardial  inflammation  is  extensive,  it  is  liable 
to  involve  to  a  certain  extent  the  muscular  tissue  of  the 
heart.  When  this  occurs,  there  will  be  cardiac  palpitation. 
The  patient  usually  will  complain  of  this  palpitation,  and 
if  the  hand  is  placed  over  the  precordial  space  it  will  be  very 
apparent.  In  some  instances  it  may  be  apparent  to  the 
physician,  when  it  is  not  appreciated  by  the  patient. 

The  pulse  usually  is  sharp  and  quick,  and  sometimes 
irregular,  for  the  action  of  the  heart  may  be  irregular  as 
well  as  excited. 

The  force  of  the  pulse  will  not  correspond  to  the  activity 
of  the  heart,  for  when  the  inflammation  has  affected  the 
muscular  structure  of  the  heart,  its  propelling  power  ia 
diminished,  and  the  pulse  becomes  feeble  and  easily  com- 
pressed. These  symptoms,  occurring  in  the  course  of  artic- 
ular rheumatism,  lead  to  the  suspicion  of  endocarditis. 

Patients  with  endocarditis  rarely  suffer  pain  or  inconveni- 
ence from  motion,  and  can  rest  on  either  side ;  the  respira- 
tion may  be  somewhat  accelerated,  but  the  dyspnoea  is 
slight,  usually  the  patient  will  only  complain  of  a  sensation 
of  weakness. 

The  temperature  rarely  rises  above  103°  F. ;  but  as  in  most 
cases  the  endocarditis  occurs  during  the  active  period  of 
some  other  disease,  it  is  difficult  to  determine  how  far  the 
rise  in  temperature  is  due  to  the  endocardial  inflammation, 
or  how  much  it  depends  upon  variations  in  the  primary 
disease. 


314  PHYSICAL   SIGKS. 

The  objective  symptoms  of  endocarditis  being  so  few  and 
equivocal,  and  the  affection  rarely  running  its  course  in  a 
well-defined  manner,  like  inflammations  of  other  important 
organs,  the  physical  signs  upon  which  you  will  be  compelled 
to  rest  for  a  diagnosis  are  all-important.  In  most  instances 
the  disease  will  go  unrecognized,  if  a  physical  exploration 
of  the  chest  is  neglected. 

PHYSICAL  SIGHTS. — At  the  commencement  of  an  attack  of 
acute  endocarditis,  on  inspection  you  will  notice  that  the 
area  of  the  visible  impulse  of  the  heart  is  increased,  and  its 
action  irregular  ;  later  it  may  become  indistinct. 

On  palpation,  at  first  the  cardiac  impulse  is  increased  in 
force ;  but  later,  when  the  walls  of  the  heart  are  weakened 
by  the  extension  of  the  inflammation,  the  force  of  the  apex- 
beat  will  be  diminished. 

Upon  percussion  the  area  of  the  precordial  dulness  re- 
mains normal  until  the  cavities  of  the  heart  become  dis- 
tended with  blood,  on  account  of  the  feebleness  of  the 
cardiac  walls ;  then  there  will  be  a  slight  increase  in  the 
precordial  dulness  beyond  the  normal  area. 

Auscultation  furnishes  the  most  important  and  constant 
sign  of  endocarditis — that  is,  a  systolic  murmur  usually 
heard  with  greatest  intensity  at  the  apex ;  this  murmur 
may  be  ventricular  or  valvular.  In  both  cases  the  murmur 
is  due  to  an  obstruction  to  the  current  of  the  blood,  which 
obstruction  is  the  result  of  thickening  or  roughening  of  the 
endocardium.  When  produced  at  the  mitral  or  tricuspid 
orifice,  the  valves  are  slightly  insufficient  on  account  of  the 
tumefied  condition  of  their  edges,  and  a  shortening  of  the 
chordae  tendinese.  When  produced  at  the  aortic  orifice,  or 
in  the  ventricle,  it  is  due  to  roughening  of  the  endocardium 
lining  the  ventricle  or  covering  the  aortic  valves. 

If,  while  you  are  watching  the  progress  of  a  case  of  acute 
articular  rheumatism,  or  any  other  disease  in  which  endo- 
carditis may  occur  as  a  complication,  a  soft,  blowing, 
systolic  murmur  is  heard  with  greatest  intensity  at  the  apex 
of  the  heart,  or  over  the  aortic  valves,  the  intensity  of 
which  has  been  gradually  increasing,  you  may  be  very  cer- 
tain that  endocarditis  is  present. 


ACUTE   ENDOCARDITIS.  315 

It  is  important  at  your  first  visit  to  a  patient  with  acnte 
articular  rheumatism,  that  you  make  a  careful  examination 
of  the  heart,  for  the  purpose  of  determining  the  existence  or 
non-existence  of  cardiac  murmurs.  If,  at  your  visit,  no 
cardiac  murmurs  are  present,  and  subsequently  a  systolic 
murmur  is  developed,  which  continues  for  two  or  three 
weeks,  and  gradually  disappears,  then  your  patient  has  had 
an  attack  of  endocarditis.  Again,  at  your  first  visit  you 
may  find  a  murmur  already  existing  ;  perhaps  you  do  not 
see  the  patient  until  a  number  of  weeks  after  the  commence- 
ment of  the  rheumatic  attack  ;  but  if  the  murmur  is  systo- 
lic, soft,  and  blowing  in  character,  and  if  it  gradually 
subsides  and  finally  disappears  with  the  subsidence  of  the 
rheumatism,  the  evidence  is  conclusive  that  the  patient  has 
suffered  from  an  attack  of  acute  endocarditis. 

Again,  if  at  your  first  examination  a  loud,  rough,  systolic 
murmur  is  heard,  with  an  increase  in  the  force  and  area  of 
the  apex-beat,  showing  the  existence  of  some  cardiac  hyper- 
trophy, the  probability  is  that  the  murmur  is  not  due  to  a 
recent  endocarditis,  but  to  valvular  disease  of  long  stand- 
ing. Under  such  circumstances,  to  determine  the  existence 
of  acute  endocarditis  is  very  difficult  if  not  impossible,  for 
a  fresh  endocarditis  may  occur  on  an  old  valvular  lesion. 
If  you  find  cardiac  hypertrophy,  or  if  the  murmur  present 
indicates  extensive  regurgitation  at  either  of  the  valvular 
orifices,  the  presumption  is  that  the  murmur  is  due  to 
some  old  valvular  lesion  ;  besides,  endocardial  murmurs 
due  to  acute  endocarditis  are  not  persistent,  but  gradually 
become  indistinct  after  they  have  been  present  for  a  con- 
siderable time. 

The  valvular  changes  and  causes  of  these  murmurs,  I 
shall  consider  more  fully  under  the  head  of  cardiac 
murmurs. 

DIFFEBENTIAL  DIAGNOSIS. — As  the  diagnosis  of  endo- 
carditis rests  almost  entirely  upon  the  presence  of  an 
endocardial  murmur,  the  point  of  difficulty  in  any  given 
case  is,  to  determine  whether  the  murmur  is  of  old  or 
rocent  origin. 

If,  as  I  have  already  stated,  during  an  attack  of  acute 


316  PROGNOSIS. 

rheumatism,  an  endocardial  murmur  is  developed  under 
your  daily  examination,  it  is  almost  a  sure  index  of  acute 
endocarditis  ;  or,  if  a  murmur  exists  at  your  first  exami- 
nation, which  is  systolic,  soft,  and  blowing  in  character,  and 
not  accompanied  by  the  evidences  of  cardiac  hypertrophy, 
you  have  good  reason  to  believe  that  it  is  produced  by  an 
acute  endocardial  inflammation.  If,  on  the  other  hand,  the 
murmur  is  rough  in  quality,  diastolic,  and  cardiac  hyper- 
trophy exists,  there  is  no  evidence  of  acute  endocarditis. 

Endocarditis  can  always  be  distinguished  from  pericar- 
ditis by  observing  the  rules  already  given  for  distinguish- 
ing an  endocardial  from  a  pericardial  murmur. 

The  rules  for  distinguishing  murmurs  due  to  endocarditis 
from  purely  functional  murmurs,  will  be  given  under  the 
head  of  cardiac  murmurs. 

PROGNOSIS. — The  prognosis  in  this  disease  is  always 
good,  so  far  as  imminent  danger  to  life  is  concerned  ;  but  it 
is  bad,  as  regards  complete  recovery.  Occurring  in  rheu- 
matism and  Bright's  disease  it  is  rarely  directly  fatal ;  yet, 
complete  recovery  is  the  exception,  for  permanent  valvular 
lesions  are  almost  certain  to  follow.  When  endocarditis 
occurs  in  pyaemia,  diphtheria,  and  other  septic  conditions, 
it  is  often  a  fatal  element.  The  chief  source  of  danger  in 
this  connection  is  the  occurrence  of  embolism.  Masses  of 
fibrin  of  greater  or  less  size,  which  have  collected  on  the 
prominences  of  the  endocardium,  are  liable  to  be  detached, 
and  when  detached  they  pass  into  the  general  arterial  cur- 
rent and  are  arrested  in  some  artery  which  is  too  small  to 
allow  of  their  passage  ;  the  plug  in  the  artery  arrests  the 
circulation  beyond  the  seat  of  the  obstruction,  and  as  a 
result  infarction  or  necrosis  take  place  in  the  part  whose 
blood  supply  is  thus  arrested.  The  organs  in  which  em- 
bolism is  most  likely  to  occur,  under  such  circumstances, 
are :  first,  the  spleen ;  second,  the  kidneys ;  third,  the 
brain.  When,  in  a  patient  with  acute  endocarditis  follow- 
ing a  severe  rigor,  you  notice  disturbance  in  any  of  these 
organs,  such  as  pain  or  swelling  over  the  spleen,  pain  in 
the  loins  with  albuminuria,  or  sudden  hemiplegia,  there  is 
reason  to  believe  that  an  embolism  is  formed,  and  the  oc- 


ACUTE  ENDOCARDITIS.  317 

currence  of  an  embolism  in  acute  endocarditis  always  ren- 
ders the  prognosis  very  unfavorable.  There  is  still  another 
pathological  lesion  which  may  be  developed  in  the  course 
of  acute  endocarditis,  which  will  necessitate  an  unfavorable 
prognosis. 

It  occasionally  happens  that  ulcerations  occur  either  at 
the  free  border  or  at  the  base  of  the  valves,  and  extend 
through  their  entire  substance,  causing  more  or  less  exten- 
sive rupture  or  tearing  of  the  valves,  following  which,  an  ex- 
tensive insufficiency  of  the  valve  is  developed  within  a  few 
hours.  Ulcerative  endocarditis  usually  occurs  in  the  course 
of  those  diseases  which  are  marked  by  great  vital  depres- 
sion, and  in  which  there  is  a  tendency  to  a  typhoid  con- 
dition. When  rupture  or  tearing  of  the  valves  occurs, 
typhoid  symptoms  will  come  on  very  rapidly ;  there  will  be 
sudden  and  extreme  dyspnoea,  which  will  compel  the  pa- 
tient to  assume  the  sitting  posture ;  he  becomes  rapidly  cya- 
nosed,  and  passes  into  a  condition  of  great  distress. 

Now,  if  in  the  course  of  any  such  disease,  as  for  instance, 
pyaemia  or  diphtheria,  where  you  have  had  the  physical 
signs  of  endocarditis,  suddenly  a  harsh  regurgitant  murmur 
is  developed  either  with  the  first  or  second  sound  of  the 
heart,  attended  by  symptoms  such  as  I  have  just  men- 
tioned, you  may  be  very  certain  that  ulcerative  endocarditis 
is  present,  and  the  prognosis  becomes  very  unfavorable. 
Under  such  circumstances,  acute  endocarditis  may  prove 
fatal  in  a  few  days,  or  even  in  a  few  hours. 

TREATMENT. — The  treatment  of  acute  endocarditis  will  be 
determined  by  the  circumstances  under  which  it  occurs. 
If  with  rheumatism,  anti-rheumatic  remedies  must  be  vigor- 
ously used.  If  with  pyaemia,  diphtheria,  and  septic  condi- 
tions, brandy,  quinine,  and  iron  should  be  freely  adminis- 
tered. The  occurrence  of  the  endocarditis  indicates  the 
necessity  of  a  vigorous  use  of  all  these  agents.  If  it  occurs 
in  the  exanthematous  and  essential  fevers,  it  is  impor- 
tant that  the  temperature  of  the  body  be  kept  as  low  as 
possible.  If  it  occurs  in  connection  with  Blight's  disease, 
all  those  means  which  assist  in  the  rat>id  removal  of  urea 
from  the  circulation  must  be  resorted  to. 


318  TKEATMENT. 

In  general  terms,  the  condition  in  which  the  endocarditis 
may  have  been  developed  must  form  the  basis  of  treatment. 
At  the  same  time,  you  must  remember  that  it  is  all-impor- 
tant that  patients  suffering  with  this  disease  should  be  kept 
absolutely  quiet  in  bed.  Opium  may  be  given  in  moderate 
doses  to  secure  rest,  but  it  must  not  be  administered  in  full 
doses  as  in  pericarditis.  The  patient  should  be  kept  quiet 
not  only  during  the  acute  stage  of  the  inflammation,  but 
during  the  period  of  convalescence.  During  the  entire 
period  of  the  inflammation,  the  temperature  of  the  room 
should  never  fall  below  70°  F.  The  chest  should  be  covered 
with  flannel,  and  as  little  exposed  as  possible  during  your 
physical  examination  of  the  heart.  This  class  of  patients 
should  be  furnished  with  the  most  concentrated  nutrition, 
not  only  during  the  active  progress  of  the  inflammation, 
but  subsequently  during  the  period  of  convalescence. 

If  the  action  of  the  heart  becomes  feeble,  digitalis  may  be 
administered.  Iodide  of  potassium  has  been  recommended 
to  promote  the  absorption  of  the  fibrin ous  exudation,  and 
thus  prevent  subsequent  induration  of  the  valves.  The 
valvular  induration  is  not  due  to  the  fibrinous  material,  but 
to  connective-tissue  formations ;  consequently,  on  theoreti- 
cal grounds,  the  potassium  becomes  of  doubtful  efficacy, 
and  experience  warrants  a  like  conclusion. 

Rest,  opium,  iron,  and  the  most  nutritious  diet,  with  oc- 
casional use  of  stimulants,  constitute  the  most  serviceable 
agents  to  be  employed  in  the  treatment  of  this  affection. 

Before  passing  to  the  subject  of  chronic  endocarditis,  I 
will  say  a  few  words  concerning  that  acute  ulcerative  form 
of  endocarditis,  the  pathological  changes  of  which  I  have 
already  described. 

It  always  occurs  under  conditions  of  grave  blood-poison- 
ing, as  in  puerperal  fever  and  pyaemia.  It  is  often  accom- 
panied by  pericarditis  and  pneumonia,  and  infarction  of  the 
lungs  and  other  organs.  It  is  ushered  in  by  chills,  followed 
by. high  fever,  headache,  and  great  prostration ;  the  pulse 
ranges  from  90  to  150  beats  per  minute,  and  the  tempera- 
ture sometimes  rises  as  high  as  107°  F.  The  tongue  soon 
becomes  dry,  and  the  patient  rapidly  passes  into  a  typhoid 


ACUTE   E1STDOCAEDITIS.  319 

state.  In  many  cases  there  is  jaundice,  enlarged  spleen, 
and  the  urine  is  scanty,  high-colored,  and  albuminous.  The 
heart-sounds  are  obscured,  and  a  loud  systolic,  and  some- 
times a  diastolic  murmur  is  heard,  and  the  rhythm  of  the 
heart' s  action  is  disturbed.  The  prognosis  is  bad ;  these 
cases  usually  terminate  fatally. 

This  form  of  endocarditis  is  liable  to  be  mistaken  for 
typhoid  fever  ;  but  the  evidences  of  endocarditis  become  so 
marked  as  the  disease  advances,  that  it  is  hardly  possible 
for  the  careful  observer  to  confound  the  two  diseases. 

In  its  treatment,  large  doses  of  quinine  and  stimulants 
are  the  only  means  that  seem  to  have  any  control  over  its 
progress. 


LECTURE   XXVII. 


CHRONIC  ENDOCARDITIS. 

Valvular  Murmurs  and  their  relation  to  Valvular  Diseases. — Aortic 
Obstruction. 

CHRONIC  endocarditis,  which  will  first  occupy  our  atten- 
tion this  morning,  differs  from  acute  in  the  character  of  the 
anatomical  changes  which  the  endocardium  undergoes ;  it 
is  distinctly  a  parenchymatous  inflammation. 

The  tendency  in  acute  endocarditis  is  to  thickening  and 
softening  of  the  endocardium,  especially  its  valvular  por- 
tion ;  while  in  chronic  endocarditis  the  anatomical  changes 
are  marked  by  thickening  and  induration,  rather  than 
softening  of  the  endocardium  ;  these  chronic  changes  gen- 
erally have  an  acute  origin.  There  is  no  part  of  the  endo- 
cardium that  is  exempt  from  chronic  endocardial  inflamma- 
tion ;  there  are,  however,  two  favorite  situations  for  its 
development :  namely,  that  portion  of  the  endocardium 
covering  the  valves,  and  that  portion  lining  the  apex  of  the 
left  ventricle.  Accompanying  inflammation  of  that  portion 
of  the  endocardium  covering  the  mitral  and  tricuspid  valves, 
there  is  usually  inflammation  of  the  endocardium  covering 
the  chordse  tendinese.  Most  patients  with  chronic  endo- 
carditis have  a  rheumatic  history. 

MORBID  ANATOMY. — Under  this  head  we  will  first  study 
the  anatomical  changes  which  take  place  at  the  different 
valvular  orifices  as  the  result  of  chronic  endocarditis. 

These  anatomical  changes  may  be  arranged  under  four 
heads : 


CHRONIC   ENDOCAEDITIS.  321 

First :  thickening. 
Second :  retraction. 
Third:  adhesion. 
Fourth :  degeneration. 

The  thickening  is  the  immediate  result  of  connective- 
tissue  increase,  and  is  generally  most  marked  at  the  base  of 
the  valves  and  along  the  line  of  contact. 

The  degree  of  thickening  varies ;  in  some  instances  it  is 
so  slight  as  not  to  interfere  with  the  functional  activity  of 
the  valves  ;  in  other  instances  the  valves  are  so  thickened, 
roughened,  and  hardened,  that  their  functional  activity  is 
greatly  impaired,  or  entirely  destroyed. 

The  retractions  of  the  valves  which  occur,  are  the  neces- 
sary result  of  changes  which  take  place  in  all  new  connec- 
tive-tissue formations.  As  the  new  connective  tissue,  which 
produces  the  thickening  already  referred  to,  becomes  more 
and  more  fibroid,  it  contracts,  and  as  the  contraction  goes 
on,  the  valves  become  rigid,  and  are  diminished  in  depth, 
and  present  a  puckered  appearance  ;  their  edges  become 
rounded,  hard,  and  incompressible,  having  a  cartilaginous 
feel. 

These  changes  are  generally  most  frequent  and  most 
marked  in  the  mitral  valves,  and  the  thickening  and  con- 
traction take  place  not  only  in  the  valves,  but  at  the  base  of 
the  valves  and  around  the  valvular  orifices ;  they  also 
extend  along  the  endocardial  covering  of  the  chordae  tendi- 
nese,  and  by  the  contraction  of  the  tendinous  chords  which 
they  produce,  draw  down  the  free  edges  of  the  valves, 
until,  in  some  instances,  they  become  fastened  to  the  wall 
of  the  ventricle  by  a  short  tendinous  cord. 

When  such  retractions  occur,  the  function  of  the  valves 
becomes  seriously  impaired,  permitting  extensive  regurgita- 
tion. 

Adhesions  of  the  valves  are  generally  found  in  connection 
with  retractions.  These  adhesions  commence  at  the  ex- 
treme edges  of  the  valves,  where  they  come  in  contact, 
and  gradually  unite  them,  until  all  trace  of  the  valves  is 
lost,  and  either  there  is  a  firm  curtain  with  a  small  opening 
in  it,  separating  the  auricle  from  the  ventricle,  or  the  valves, 
21 


322  3IOEBID   AXAT03IY. 

with  their  cords  and  muscles,  are  drawn  together  into  a 
perforated  cone ;  sometimes  the  closure  of  the  orifice  is  so 
complete  that  a  mere  slit  remains,  termed  a  "button-hole 
orifice."  These  contractions  are  confined  almost  exclusively 
to  the  mitral  and  aortic  orifices,  and  are  termed  mitral  and 
aortic  stenosis. 

The  degree  of  stenosis  at  these  orifices  varies  very  much 
in  different  cases.  Sometimes  the  mitral  orifice,  which  in 
a  normal  condition  readily  admits  three  fingers,  becomes  so 
much  contracted  as  hardly  to  admit  the  little  finger.  I 
have  seen  stenosis  of  the  aortic  orifice  so  extensive  as  only 
to  admit  the  end  of  the  little  finger. 

Stenosis  of  the  tricuspid  orifice  very  rarely  occurs. 

I  now  come  to  the  last  change  mentioned,  namely,  degen- 
eration of  tlie  valves.  With  or  without  the  valvular 
changes  already  described,  when  the  new  connective-tissue 
elements  have  existed  some  time,  they  undergo  degenera- 
tion. The  process  is  accomplished  as  follows :  after  the 
cell  formations  in  the  endocardium  has  been  going  on  some 
time,  and  the  new  tissue  formations  have  reached  a  certain 
point,  fatty,  granular,  or  calcareous  degeneration  of  the 
new  tissue  takes  place,  and  there  is  formed  in,  or  under- 
neath the  endocardium,  patches  of  fatty,  granular,  or  cal- 
careous substance.  Over  these  patches  the  inner  layer  of 
the  endocardium  may  be  destroyed,  and  the  patches  remain 
exposed,  or  they  may  soften  and  be  removed  by  ulceration  ; 
their  removal  is  usually  followed  by  extensive  destruction 
of  tissue,  causing  rupture  of  the  valves  and  consequent 
regurgitation.  Under  such  circumstances,  rupture  of  the 
valves  becomes  one  of  the  anatomical  changes  of  chronic 
endocarditis. 

Sometimes  the  valves  become  fixed  and  rigid,  with  little 
contraction  or  adhesion ;  the  whole  valvular  orifice  has  a 
hard,  cartilaginous  feel,  and  from  the  rigid  free  edges 
tubercles  of  chalky  matter  extend  into  the  orifice,  as  well 
as  into  the  cardiac  cavities.  Mitral  stenosis  and  calcareous 
degeneration  are  rarely  associated. 

Calcareous  degeneration  is  generally  more  abundant  at 
the  aortic  than  at  the  mitral  orifice.  The  reason  for  this 


CIIEOXIC   ENDOCARDITIS.  323 

may  perhaps  be  found  in  the  fact  that  the  changes  at  the 
aortic  opening  generally  occur  at  a  later  period  in  life  than 
those  which  occur  at  the  mitral  opening. 

Changes  at  the  aortic  orifice  are  usually  not  very  exten- 
sive until  after  middle  life,  while  those  at  the  mitral  open- 
ing most  frequently  occur  in  young  persons,  and  they  rarely 
produce  as  much  insufficiency,  thickening,  retraction  or 
adhesion. 

There  is  one  thing  more  which  I  have  purposely  omitted 
until  now,  in  order  that  you  may  not  be  misled  by  the 
statement,  namely,  that  the  thickening  of  the  endocardium 
in  chronic  endocarditis  takes  place  in  the  endocardial  tissue  ; 
it  is  not  a  surface  process,  but  a  growth — an  increase  of  tis- 
sue in  and  underneath  the  endocardium.  Whenever  a  prom- 
inence occurs  at  any  point  on  the  surface  of  the  valves  by 
an  increase  in  the  thickness  of  the  endocardium,  that  eleva- 
tion becomes  the  site  for  a  fibrinous  deposit  from  the  blood. 
You  will  therefore  have  in  chronic  endocarditis  these  fibrin- 
ous deposits  taking  place,  sometimes  half  an  inch  or  more 
in  length.  These  deposits  are  the  so-called  vegetations, 
and  they  are  very  liable,  in  rheumatic  patients,  to  be  de- 
veloped in  connection  with  thickening  and  retraction  of  the 
valves.  These  deposits  interfere  more  or  less  with  the  func- 
tion of  the  valves,  and  if,  at  the  aortic  orifice,  they  become 
adherent  to  the  walls  of  the  aorta,  they  may  cause  a  sudden 
and  rapidly  fatal  regurgitation.  As  in  acute  endocarditis, 
the  separation  of  a  portion  of  these  deposits  may  give  rise 
to  embolism,  which  causes  the  development  of  infarction 
and  necrosis  in  some  of  the  vital  organs. 

Thus  a  great  variety  of  valvular  changes  may  be  pro- 
duced during  the  progress  of  a  chronic  endocarditis,  and 
one  or  all  of  the  valves  of  the  heart  may  be  involved  in  these 
changes.  The  valves  which  are  most  frequently  involved  in 
a  rheumatic  chronic  endocarditis  are  the  mitral ;  while  in 
that  form  which  occurs  in  advanced  life  the  aortic  valves 
are  most  frequently  involved. 

When  chronic  endocarditis  has  its  seat  in  that  portion  of 
flie  endocardium  lining  the  cavity  of  the  ventricle,  it  does 
not  give  rise  to  elevation,  but  rather  depression,  which 


324  MORBID   ANATOMY. 

passes  by  slow  degrees  into  bulging.  The  endocardium  at 
the  seat  of  the  inflammatory  processes  assumes  a  fibroid 
appearance  ;  with  the  depression  that  occurs  in  the  tissues 
at  the  point  of  its  development,  there  is  an  increase  of  con- 
nective tissue,  but  the  increase  takes  place  at  the  expense 
of  the  muscular  structure  of  the  heart.  This  connective- 
tissue  increase  and  disappearance  of  the  muscular  wall  of 
the  heart  may  be  developed  to  such  an  extent  that  the 
entire  cardiac  wall  at  that  point  may  become  a  mass  of 
fibroid  tissue,  and  what  has  been  termed  aneurism  of  the 
heart  may  be  developed  as  a  result. 

This  change  is  not  a  fibrous  degeneration  of  the  muscular 
structure,  but  it  is  a  fibrous  outgrowth,  and  is  generally 
most  extensive  at  the  apex  of  the  left  ventricle.  In  cutting 
into  these  fibrous  spots,  which  may  vary  in  size  from  half 
an  inch  to  an  inch  in  diameter,  you  will  find  them  made  up 
of  firm  fibrous  tissue,  which  sometimes  extends  through  the 
entire  thickness  of  the  cardiac  walls.  The  chordae  tendinea3 
of  the  mitral  valves,  as  well  as  the  columnse  carnese  (the 
latter  belonging  to  the  muscular  structure  of  the  heart),  are 
not  unfrequently  found  shortened,  thickened,  and  con- 
tracted to  such  a  degree  as  to  prevent  the  closure  of  the 
valves,  and  thus  render  them  insufficient.  The  changes 
which  produce  these  contractions  and  shortenings  are  the 
result  of  inflammatory  changes  analogous  to  those  which 
give  rise  to  thickness,  contraction,  and  shortening  of  valves. 

SYMPTOMS. — There  are  no  positive  objective  symptoms  of 
chronic  endocarditis, — there  may  be  certain  uneasy  sensa- 
tions about  the  heart,  with  palpitation,  but  they  are  in  no 
way  diagnostic. 

Clinically,  we  only  know  of  its  existence  by  the  changes 
which  it  produces  in  the  valves  and  valvular  orifices,  which 
give  rise  to  changes  in  the  sounds  of  the  heart ;  but  the  ab- 
normal heart-sounds,  which  are  indicative  of  the  valvular 
changes  produced  by  chronic  endocarditis,  do  not  differ  from 
those  produced  by  other  valvular  lesions. 

The  abnormal  heart-sounds  indicative  of  valvular  changes 
in  chronic  endocarditis  will  be  fully  considered  in  connec- 
tion with  the  study  of  valvular  murmurs. 


CHRONIC   ENDOCARDITIS.  325 

PROGNOSIS. — The  prognosis  in  chronic  endocarditis  will 
depend  altogether  upon  the  seat  and  extent  of  the  valvular 
lesions.  When  there  is  simple  thickening  of  the  valves, 
without  retraction  or  deposit  upon  their  surface,  the  progno- 
sis may  be  very  good.  Again,  extensive  valvular  changes 
may  exist  at  one  orifice  which  may  not  essentially  interfere 
with  the  cardiac  circulation,  while  the  same  changes  at 
another  orifice  may  give  rise  to  very  great  disturbance  in 
the  general  circulation. 

I  shall  more  fully  consider  the  prognosis  of  these  dif- 
ferent valvular  lesions  under  the  head  of  cardiac  murmurs. 

TREATMENT. — The  treatment  of  chronic  endocarditis  will 
also  be  determined  by  the  location  and  extent  of  the  valvu- 
lar clianges.  The  general  rule  for  its  management  is,  to 
remove  the  exeiting  cause.  If  the  patient  is  a  rheumatic 
subject,  if  possible  he  should  make  his  residence  where  he 
will  be  free  from  rheumatic  developments.  With  every  rheu- 
matic attack,  there  will  be  an  increase  of  the  endocardia! 
inflammation,  and  more  extensive  thickening  and  retraction 
will  take  place  at  the  valvular  orifices.  This  class  of  pa- 
tients must  be  removed  from  all  excitement,  and  alcoholic 
stimulants  are  by  all  means  to  be  avoided  ;  all  active  phy- 
sical exercise  must  be  stopped,  and  the  surface  of  the  body 
must  be  carefully  protected  from  exposure  to  sudden  varia- 
tions in  temperature.  The  diet  should  be  most  nutritious 
and  non-stimulating. 

The  special  treatment  which  is  to  be  followed  in  the  man- 
agement of  each  valvular  lesion  will  be  fully  considered  un- 
der the  head  of  valvular  murmurs. 

VALVULAR   MURMURS,   AND    THEIR  RELATION   TO   VALVULAR 

DISEASES. 

The  valvular  lesions  already  described  as  occurring  in  the 
course  of  acute  and  chronic  endocarditis  furnish  signs  by 
which  they  may  be  recognized  during  life.  The  study  of 
these  signs  in  connection  with  the  anatomical  changes  which 
produce  them,  will  now  engage  our  attention. 

These  anatomical  changes  are  of  two  kinds.  First :  Val- 
vular thickenings  with  slight  retraction,  valvular  adhesions, . 


326  MORBID   AXATOMY. 

regurgitation,  and  atheromatous  and  calcareous  degenera- 
tion ;  any  one  of  these  changes  may  prevent  the  valve? 
from  being  accurately  applied  to  the  walls  of  the  artery,  or 
to  the  walls  of  the  ventricles,  and  thus  diminish,  more  or 
less,  the  size  of  the  valvular  orifices,  and  offer  obstacles  to 
the  current  of  blood.  The  impinging  of  the  blood-current 
against  the  obstacles,  gives  rise  to  sounds  called  obstructive 
murmurs,  and  constitutes  the  causes  of  obstruction  to  the 
current  of  blood  as  it  passes  through  the  orifices  and 
cavities  of  the  heart. 

Second:  Extensive  valvular  retraction,  perforation,  and 
partial  detachment  of  the  valves,  and  rupture  of  the  chordae 
tendinese,  and  the  formation  of  calcareous  plates  in  the 
valves  and  around  the  valvular  orifices,  prevent  the  valves 
from  completely  closing  their  respective  orifices  ;  an  opening 
is  consequently  left,  through  which  the  blood  returns  into 
the  cavity  from  which  it  has  just  been  expelled,  giving  rise 
to  a  condition  called  insufficiency. 

These  two  alterations  generally  coexist,  one  usually  being 
more  extensive  than  the  other ;  as,  for  instance,  the  obstruc- 
tion may  be  slight  and  the  regurgitation  extensive ;  or,  the 
obstruction  may  be  extensive  and  the  regurgitation  slight. 
The  effect  of  these  valvular  deformities  depends  entirely 
upon  their  seat.  While  they  are  attended  with  little  appa- 
rent disturbance  of  the  circulation  at  one  valvular  orifice,  at 
another  orifice  they  very  rapidly  bring  the  circulation  into 
an  unmanageable  condition. 

I  shall  speak  separately  of  the  effects  of  these  different 
anatomical  changes  at  the  different  valvular  orifices,  begin- 
ning with  the  aortic  orifice. 

AORTIC  OBSTRUCTION. 

This  is  a  very  common  form  of  heart  disease,  and  is  fre- 
quently associated  with  more  or  less  regurgitation.  It  is 
always  accompanied  by  some  hypertrophy  of  the  ventricular 
walls. 

MORBID  ANATOMY. — The  lesions  which  give  rise  to  aortic 
obstruction  are  those  changes  which  take  place  in  the  aorti^ 
valves  and  at  the  aortic  orifice  during  the  progress  of  acute 


AOETIC   OBSTRUCTION.  327 

and  chronic   endocarditis,  as  well  as  with  atheromatous 
degeneration  of  these  valves. 

In  some  cases  the  valves  which  have  become  thickened 
and  rigid  from  chronic  endocarditis,  or  from  atheromatous 
or  calcareous  degeneration,  cannot  be  pressed  back  against 
the  wall  of  the  aorta,  and  by  protruding  into  the  current  of 
the  circulation,  so  obstruct  the  current  of  blood  as  it  passes 
from  the  ventricle  into  the  aorta,  that  a  rough  murmur  is 
produced  which  occupies  or  takes  the  place  of  the  whole  of 
the  first  sound  of  the  heart. 

In  other  cases,  adhesions  of  the  valves  and  increase  of 
connective  tissue  at  their  base,  with  the  development  of 
calcareous  plates  underneath,  and  vegetation  on  the  surface 
of  thickened  endocardium,  may  almost  entirely  close  the 
orifice,  and  give  rise  to  very  great  obstruction  to  the  out- 
going current  of  blood.  I  have  seen  stenosis  of  the  aortic 
orifice  produced  in  this  way  to  such  an  extent  as  to  almost 
entirely  close  the  opening.  As  a  result  of  such  stenosis,  in 
order  to  propel  the  blood  through  the  constricted  orifice,  the 
left  ventricle  is  called  upon  to  perform  an  abnormal  amount 
of  labor,  which  necessarily  leads  to  more  or  less  extensive 
hypertrophy  of  its  walls. 

Again,  a  slight  thickening  of  the  valvular  endocardium 
may  be  accompanied  by  vegetations  on  the  surface  of  the 
valves,  which  will  cause  very  loud  obstructive  murmurs, 
and  yet  not  materially  interfere  with  the  cardiac  circu- 
lation. 

Aortic  obstruction  may  be  due  to  any  one  or  to  all  of  the 
anatomical  changes  to  which  I  have  just  referred ;  but, 
when  the  obstruction  is  due  to  stenosis  of  the  orifice  its 
effects  are  very  different  from  those  which  we  have  when  a 
slight  roughening  or  thickening  of  a  valve  causes  the  ob- 
struction. If  the  orifice  has  become  very  much  narrowed, 
so  that  the  whole  current  of  the  blood  must  be  forced 
through  a  very  narrow  opening,  it  is  very  easy  to  under- 
stand that  the  disturbance  of  the  general  circulation  would 
be  very  much  greater  and  would  be  productive  of  far  more 
serious  results,  than  if  the  obstruction  was  due  to  the  pres- 
ence of  slight  thickening  or  roughening  of  the  valves,  which 


828  ETIOLOGY. 

would  cause  very  little  interference  to  the  passage  of  blood 
from  the  ventricle  into  the  aorta. 

The  cardiac  hypertrophy  which  is  developed  as  the  result 
of  aortic  stenosis,  comes  on  gradually,  and  is  not  attended 
by  dilatation  of  the  ventricular  cavity  ;  it  is  simply  a  hyper- 
trophy of  the  walls  of  the  left  ventricle.  After  a  time, 
insufficiency  of  the  mitral  valves  is  apt  to  follow,  caused 
by  an  extension  of  the  endocardia!  inflammation  from  the 
aortic  valves,  or  by  the  forcible  pressure  of  blood  upon  the 
ventricular  surface  of  the  valves. 

ETIOLOGY. — Aortic  obstruction  is  most  frequently  met 
with  in  middle  and  advanced  life,  and  may  originate  (as 
I  have  already  stated)  in  acute  or  chronic  endocarditis,  or 
in  atheromatous  and  calcareous  degeneration.  The  aortic 
valves  are  sometimes  affected  in  those  who  are  subjected 
to  prolonged  and  severe  muscular  effort. 

Atheromatous  degeneration  commencing  in  the  aorta,  if 
at  all  extensive,  after  a  time  involves  the  aortic  valves  and 
orifice,  giving  rise  not  only  to  obstruction  to  the  outgoing 
current  of  blood,  but  to  regurgitation. 

These  aortic  valves  sometimes  become  the  seat  of  a  pecu- 
liar form  of  degeneration  in  the  advanced  stage  of  syphilis, 
the  anatomical  changes  of  which  resemble  those  of  chronic 
endocarditis ;  the  inflammatory  changes  are  accompanied, 
however^  by  granular  deposits  peculiar  to  syphilis.  With 
these  changes  there  is  also  more  or  less  aortic  obstruction. 

SYMPTOMS. — A  state  of  comparative  good  health  is  com- 
mon in  persons  with  aortic  obstruction.  Generally  the 
pulse  is  small,  compressible,  jerking  in  character,  and 
sometimes  intermittent.  The  arteries  are  scantily  filled, 
whfle  the  veins  are  overcharged.  The  countenance  is  pale, 
and  this  class  of  patients  are  liable  to  fits  of  syncope,  on 
account  of  cerebral  anaemia.  There  is  no  evidence  of  any 
obstruction  in  the  pulmonary  circulation  until  the  mitral 
orifice  has  become  secondarily  involved.  It  is  remarkable 
to  what  an  extent  aortic  stenosis  may  be  carried  without 
materially  interfering  with  the  systemic  circulation,  or 
giving  rise  to  oedema  of  the  feet,  or  any  other  of  the  class 
of  symptoms  which  attend  such  disturbance. 


AOETIC   OBSTRUCTION.  329 

You  must  remember  that  particles  of  fibrin  are  very  liable 
to  be  detached  from  the  valves  when  vegetations  are  the 
cause  of  the  obstruction,  and  these  masses  may  give  rise  to 
embolism  in  some  organ  removed  from  the  heart,  especially 
the  brain. 

PHYSICAL  SIGXS. — The  physical  signs  of  aortic  obstruc- 
tion are  generally  distinctive,  and  easily  appreciated. 

Upon  inspection,  the  visible  area  of  the  cardiac  impulse 
is  abnormally  increased. 

By  palpation,  the  force  of  the  cardiac  impulse  will  not 
only  be  found  increased,  but  in  many  instances  it  will  have 
a  heaving  character,  and  be  felt  farther  to  the  left  than 
normal. 

Upon  percussion  there  will  be  an  increased  area  of  dul- 
ness  to  the  left,  corresponding  to  the  altered  apex-beat ; 
also  corresponding  to  the  degree  of  hypertrophy  of  the  left 
ventricle,  and  the  increase  will  not  only  be  to  the  left,  but 
downward. 

Upon  auscultation  a  murmur  will  be  heard  synchronous 
with  the  first  sound  of  the  heart,  directly  over  the  normal 
position  of  the  aortic  valves,  behind  the  sternum,  at  the 
junction  of  the  third  rib  with  the  sternum.  This  murmur 
has  its  maximum  of  intensity  at  the  second  sterno-costal 
articulation  upon  the  right  side ;  it  is  conveyed  up  the 
aorta  to  the  carotids,  and  may  be  heard  with  diminished 
intensity  over  the  whole  cardiac  region.  It  is  usually  harsh 
in  character,  and  more  or  less  obscures  the  first  sound  of 
the  heart ;  it  may  entirely  replace  it,  or  the  first  sound  may 
be  heard  and  then  the  murmur  following. 

If  there  is  no  regurgitation,  the  aortic  second  sound  will 
be  feeble  or  inaudible,  while  the  second  sound  over  the  pul- 
monic  valves  will  be  intensified.  The  tracings  of  the  sphyg- 
mograph  are  so  uncertain,  that  I  regard  the  instrument  of 
little  aid  in  diagnosis  or  prognosis  in  cardiac  diseases.  I 
shall  not,  therefore,  make  mention  of  the  different  tracings 
which  it  has  been  claimed  indicate  the  existence  of  differ- 
ent forms  of  cardiac  disease. 


LECTURE    XXVIII. 


VALVULAR   LESIONS. 


Aortic  Obstruction. — Aortic  Regurgitation. 

THIS  morning  I  will  continue  the  history  of  aortic  obstruc- 
tion by  inviting  your  attention  to  its  differential  diagnosis. 

DIFFERENTIAL  DIAGNOSIS. — The  diagnosis  of  aortic  ob- 
struction mainly  rests  upon  the  presence  of  a  systolic  aortic 
murmur.  This  murmur  may  be  confounded  with  a  mitral, 
tricuspid,  or  regurgitant,  or  with  an  anaemic  bruit. 

It  may  be  distinguished  from  a  mitral  regurgitation  by 
the  points  at  which  the  murmur  is  heard  with  its  maximum 
intensity,  and  its  area  of  diffusion.  Both  aortic  obstruction 
and  mitral  regurgitation  are  accompanied  by  systolic  mur- 
murs. An  aortic  obstructive  murmur  may  be  heard  at  the 
apex  and  over  the  anterior  portion  of  the  chest,  but  its 
point  of  maximum  intensity  is  at  the  second  sterno-costal 
articulation  on  the  right  side  ;  whereas,  with  mitral  regur- 
gitation, the  murmur  has  its  point  of  maximum  intensity  at 
the  apex-beat ;  it  may  be  audible  at  the  base  of  the  heart, 
but  with  very  much  less  intensity  than  at  the  apex.  The 
area  of  diffusion  of  a  mitral  regurgitant  murmur  is  toward 
the  left  and  backward. 

Aortic  obstruction  may  be  distinguished  from  tricuspid 
regurgitation  from  the  fact  that  the  point  at  which  an  aortic 
obstructive  murmur  is  heard,  with  its  maximum  intensity,  is 
at  the  second  sterno-costal  articulation,  while  a  tricuspid 
regurgitant  murmur  has  its  maximum  of  intensity  at  the 
apex,  and  is  rarely  audible  above  the  junction  of  the  third 
rib  with  the  sternum. 


AORTIC    OBSTRUCTION.  331 

In  conditions  of  anaemia  a  murmur  is  heard  exactly  cor- 
responding in  rhythm  and  seat  with  an  aortic  obstructive 
murmur.  An  anaemic  murmur,  however,  does  not  generally 
have  its  maximum  of  intensity  at  the  junction  of  the  second 
rib  with  the  sternum,  but  is  heard  with  greatest  intensity 
over  the  carotids,  and  it  will  be  attended  by  a  more  or  less 
marked  venous  hum.  Again,  with  aortic  obstruction  there 
is  usually  some  cardiac  hypertrophy,  with  increased  force 
of  the  apex -beat ;  whereas,  in  anaemia,  the  cardiac  impulse 
is  feeble.  The  radial  pulse  in  aortic  obstruction  is  jerking 
in  character,  and  gives  to  the  finger  a  sensation  of  hardness  ; 
in  anaemia,  the  pulse  is  soft,  full,  and  compressible.  Then 
you  have  the  other  general  phenomena  of  anaemia,  and 
although  they  are  sometimes  present  in  connection  with 
aortic  obstruction,  yet,  if  you  take  into  consideration  the 
changes  in  the  ventricular  walls,  which  to  a  greater  or  less 
extent  attend  obstruction,  in  most  cases  you  will  find  it 
comparatively  easy  to  make  a  differential  diagnosis  between 
an  anaemic  bruit  and  an  aortic  obstructive  murmur. 

PROGNOSIS. — The  prognosis  in  aortic  obstruction  depends 
altogether  upon  the  extent  of  the  changes  in  the  ventricular 
walls.  I  have  already  said  that  whenever  the  obstruction 
reaches  such  a  point  as  to  materially  interfere  with  the  emp- 
tying of  the  cavity  of  the  left  ventricle,  it  will  cause  more  or 
less  hypertrophy  of  the  ventricular  walls  ;  this  hypertrophy 
commences  with  the  commencement  of  the  obstruction,  and 
increases  with  the  increase  of  the  obstruction;  thus  the 
wall  of  the  ventricle  may  be  increased  to  twice  or  three 
times  its  normal  thickness,  and  that  without  any  dilatation 
of  its  cavity.  Although  the  walls  of  the  left  ventricle  may 
in  this  way  become  greatly  hypertrophied,  if  the  rhythm  of 
the  heart's  action  is  not  destroyed,  the  prognosis  as  to  the 
duration  of  life  is  not  bad  ;  but  if,  on  violent  muscular  ex- 
ercise, there  is  a  tendency  to  interruption  of  the  heart's 
action,  there  is  danger  that  the  stoppage  of  the  ventricular 
systole  may  be  permanent,  and  sudden  death  result.  On 
the  other  hand,  if  the  ventricular  systole  becomes  feeble 
and  intermitting,  although  the  ventricular  walls  may  be 
thickened,  the  left  ventricle  becoming  over-distended  with 


832  MORBID   ANATOMY. 

blood  on  account  of  the  obstruction  to  its  passage,  and  the 
degeneration  which  has  occurred  in  the  hypertrophied  mus- 
cular tissue  of  the  ventricular  walls,  the  arterial  supply  will 
be  cut  off  from  the  brain,  and  the  patient  may  suddenly  die 
from  cerebral  anaemia. 

Again,  if  there  is  no  evidence  of  cardiac  hypertrophy,  or 
only  slight  evidence  of  its  existence,  although  the  presence 
of  an  aortic  systolic  murmur  may  indicate  that  there  is 
obstruction  at  the  aortic  orifice,  the  prognosis  will  be  good, 
especially  if  the  murmur  has  been  known  to  have  existed 
for  some  time. 

Such  murmurs,  which  have  existed  for  one  or  two  years 
without  the  development  of  hypertrophy  of  the  left  ven- 
tricle, will  probably  do  no  harm,  unless  fibrin  accumulate 
at  the  point  of  obstruction,  and  embolism  ensue. 

It  is  hardly  possible,  by  physical  signs,  to  determine  the 
presence  or  absence  of  vegetations;  if,  however,  an  aortic 
systolic  murmur  has  existed  for  one  or  two  years  without 
producing  any  marked  change  in  the  ventricular  walls,  it 
may  be  regarded  as  evidence  almost  conclusive  that  vegeta- 
tions are  not  present. 

In  any  case  of  aortic  obstruction  where  the  evidences  of 
extreme  hypertrophy  are  present,  accompanied  by  a  jerking, 
irregular  pulse,  and  where  the  patient  has  had  repeated 
attacks  of  vertigo,  attended  and  followed  by  great  muscular 
weakness,  with  extreme  pallor  of  countenance,  there  is  con- 
stant danger,  for  there  is  a  liabilit}"  at  any  time  to  sudden 
syncope,  from  which  he  may  not  rally. 

Whenever  an  aortic  stenosis  has  existed  for  a  considerable 
time,  and  from  an  extension  of  the  inflammatory  process, 
the  mitral  valves  have  become  so  involved  as  to  render 
them  insufficient,  the  prognosis  is  very  unfavorable. 

TREATMENT. — The  treatment  of  aortic  obstruction  will  be 
considered  in  connection  with  aortic  regurgitation  ;  the  two 
conditions  are  frequently  associated,  and  the  principles  of 
treatment  are  the  same. 

AORTIC  REGURGITATION. 

As  I  have  already  stated,  aortic  regurgitation  is  closely 


AOKTIC   REGUEGITATIOlSr.  333 

allied  to  aortic  obstruction  ;  both  in  its  situation,  and  in  the 
anatomical  changes  which  take  place  in  the  valves.  Aortic 
regurgitation  without  some  obstruction  is  of  rare  occurrence. 

MORBID  ANATOMY. — There  are  several  anatomical  changes 
of  the  aortic  valves  which  permit  the  regurgitation  of  blood 
during  the  cardiac  diastole.  The  semilunar  valves  either 
are  so  shrunken  and  shortened  by  chronic  endocarditis,  or 
by  an  atheromatous  process,  that  they  do  not  meet  and 
close  the  aortic  orifice,  or  the  valves  become  adherent  to  the 
aortic  wall  and  are  thus  prevented  from  closing  the  orifice, 
or  laceration  and  detachment  of  one  of  the  valves  occur,  and 
thus  a  free  opening  for  regurgitation  is  formed.  Undoubt- 
edly, the  interstitial  inflammation  which  gives  rise  to  the 
valvular  changes  which  allow  of  regurgitation,  is  sometimes 
excited  by  the  violence  with  which  the  valves  are  closed  by 
the  backward  rush  of  blood  on  the  aortic  recoil  during  pro- 
longed and  violent  physical  exertion. 

When  regurgitation  at  the  aortic  orifice  has  existed  for 
some  time,  a  new  series  of  changes  occurs.  The  blood  which 
regurgitates  through  the  aortic  orifice  is  added  to  that  which 
is  passing  normally  from  the  auricle  through  the  auriculo- 
ventricular  opening ;  by  the  combination  of  these  two 
streams,  the  left  ventricle  is  over-distended  during  its  dias- 
tole. The  result  of  this  is  dilatation  of  the  cavity  of  the  left 
ventricle  ;  for  during  the  ventricular  diastole,  the  muscular 
fibres  of  the  ventricular  walls  are  in  a  relaxed  condition, 
and  when  the  abnormal  pressure  is  brought  to  bear  by  the 
double  current  of  blood,  the  ventricle  becomes  distended 
beyond  its  normal  limits,  and  a  permanent  dilatation  of  the 
ventricular  cavity  is  soon  developed. 

Almost  immediately  with  the  dilatation  of  the  ventricle, 
hypertrophy  of  the  ventricular  walls  is  developed,  in  order 
to  resist  and  overcome  the  over-distention  of  the  ventricular 
cavity ;  or,  in  other  words,  to  overcome  the  obstruction  to 
the  cardiac  circulation.  In  this  way,  the  left  ventricle  be- 
comes dilated  and  hypertrophied. 

The  hypertrophy  goes  on  increasing,  until  it  compensates 
for  the  dilatation,  but  before  this  point  is  reached  the  ven- 
tricular cavity  sometimes  becomes  very  much  dilated,  and 


334  MORBID   ANATOMY. 

the  left  heart  attains  an  immense  size.  Under  these  circum- 
stances, the  left  ventricle  is  capable  of  receiving  and  contain- 
ing more  than  its  normal  quantity  of  blood  ;  consequently, 
with  each  cardiac  pulsation,  an  abnormal  quantity  of  blood 
is  thrown  into  the  arterial  system  which  distends  the  arteries 
beyond  their  normal  limits.  As  a  result  of  these  repeated 
and  sudden  arterial  distentions,  an  endocarditis  is  developed 
which  leads  to  atheromatous  degeneration  of  the  arterial 
walls.  This  arterial  degeneration  places  the  patient  in  a 
situation  in  which  he  is  constantly  exposed  to  danger ;  for 
during  violent  mental  excitement  or  prolonged  physical 
exertion,  an  artery  in  the  brain  is  liable  to  rupture,  and  give 
rise  to  a  cerebral  apoplexy. 

Again,  in  the  normal  condition  of  the  heart,  the  aortic 
recoil  is  the  force  which  propels  the  blood  into  the  coronary 
artery.  Now.  wdien  the  aortic  valves  are  insufficient,  they 
furnish  little  resistance  to  the  return  blood-current ;  conse- 
quently, the  flow  of  blood  into  the  coronary  vessels  is  di- 
minished and  the  coronary  arteries  receive  less  than  their 
normal  supply  of  blood.  As  a  result  of  this  interference 
with  the  coronary  circulation,  the  nutrition  of  the  hyper- 
trophied  ventricular  walls  is  interfered  with,  and  after  a 
time  they  undergo  tissue  degeneration.  Now,  dilatation  of 
the  ventricular  cavity  recommences  at  the  expense  of  the 
hypertrophied  walls ;  this  ventricular  dilatation  is  neces- 
sarily very  extensive,  and  the  mitral  valves  become  insuffi- 
cient to  close  the  dilated  auriculo-ventricular  orifice ;  and 
from  the  regurgitation  of  blood  through  the  auriculo-ven- 
tricular orifice,  you  have  obstructed  venous  circulation 
added  to  the  deficient  systemic  circulation. 

The  mitral  valves  may  also  become  insufficient  in  connec- 
tion with  aortic  regurgitation,  either  by  an  extension  of  en- 
docarditis or  an  atheromatous  process  from  the  aortic  valves, 
or  the  chordae  tendinese  may  become  shrunken  and  shortened 
by  an  extension,  or  by  the  development  of  chronic  endocar- 
ditis. This  endocarditis  is  secondary  to  the  aortic  regurgi- 
tation, and  prevents  the  valves  from  closing  the  orifice  ;  or, 
on  account  of  the  atrophy  of  the  papillary  muscles,  the  folds 
of  the  valve  during  the  ventricular  systole  are  not  prevented 


AOETIC   KEGUKGITATIOlSr.  335 

from  passing  into  the  auricle.  Thus,  in  some  one  of  these 
ways,  the  mitral  valves  often  become  insufficient  as  a  seque- 
lae of  aortic  regurgitation.  Whenever  mitral  insufficiency 
occurs,  the  symptoms  of  aortic  regurgitation  are  modified 
by  those  of  failure  of  the  mitral  valves.  Under  these  cir- 
cumstances there  arises  a  general  disturbance  of  the  venous 
circulation,  the  veins  become  distended,  cyanosis  occurs, 
and  dropsy  ensues  in  consequence  of  the  interference  of  the 
return  circulation,  which  develops  all  of  those  distressing 
phenomena  which  attend  advanced  cardiac  disease. 

ETIOLOGY. — The  causes  of  aortic  insufficiency  do  not  re- 
quire separate  consideration.  They  are  very  nearly  the 
same  as  those  which  I  named  as  causes  of  aortic  obstruction, 
viz.  :  acute  and  chronic  endocarditis,  excessive  bodily  exer- 
tion, and  atheroma  of  the  aorta.  All  of  which  have  been 
considered  in  connection  with  its  morbid  anatomy. 

We  now  come  to  the  symptoms  of  aortic  regurgitation, 
independent  of  any  other  valvular  lesion. 

SYMPTOMS. — Sometimes  persons  with  extensive  regurgita- 
tion at  the  aortic  orifice  enjoy  comparatively  good  health, 
and  suffer  no  special  inconvenience  from  their  heart-disease. 
This  occurs  only  in  those  cases  where  the  hypertrophy  of 
the  left  ventricle  fully  compensates  for  the  regurgitation,  or 
where  the  leakage  of  the  valves  is  so  slight  that  the  regurgi- 
tant  blood  is  not  sufficient  to  cause  over-distention  of  the 
ventricular  cavity.  Such  persons  do  not  even  suffer  from 
dyspnoaa  on  violent  physical  exertion  ;  there  may  be  some 
cardiac  palpitation,  but  it  is  not  constant  nor  troublesome. 

This  condition  of  apparent  health  is  usually  of  short 
duration,  for  the  causes  which  produce  the  regurgitation 
are  generally  progressive,  as  is  the  consequent  hypertrophy 
of  the  ventricular  walls.  When  the  hypertrophy  reaches  a 
certain  point,  it  gives  rise  to  an  excessive  action  of  the  heart 
under  slight  mental  excitement  or  violent  physical  exertion. 
The  patient  then  begins  to  complain  of  vertigo,  headache, 
and  spots  before  his  eyes  ;  he  becomes  anxious  and  nervous, 
and  conscious  of  the  labored  action  of  his  heart ;  he  feels 
that  active  exercise  increases  his  sufferings,  and  may  be  fol- 
lowed by  attacks  of  syncope.  His  pulse  is  slightly  ac- 


336  SYMPTOMS. 

celerated,  is  quick  and  jerking  in  character,  but  regular  in 
rhythm ;  the  radial  impulse  is  perceived  a  little  after  the 
apex- beat,  or  first  sound  of  the  heart.  In  such  cases,  it  is 
always  well  to  determine  whether  the  action  of  the  heart 
remains  regular  under  mental  excitement  or  physical  exer- 
tion ;  if  it  does,  it  is  in  a  far  better  condition  than  when  it 
becomes  irregular.  The  patient  may  go  on  for  years,  at 
times  suffering  from  dyspnoea,  giddiness,  carotid  pulsation, 
and  cardiac  palpitation,  and  obliged  to  have  his  head 
elevated  when  lying  down ;  yet  he  becomes  accustomed  to 
these  symptoms,  and  leads  a  life  of  comparative  comfort. 

After  a  time,  however,  the  degenerative  processes,  already 
described  as  taking  place  in  the  hypertrophied  ventricular 
walls  from  interference  with  their  nutrition,  take  place, 
and  the  hypertrophied  ventricle  is  no  longer  able  to  over- 
come the  impediments  to  the  circulation,  either  from  result- 
ing insufficiency  of  the  mitral  valves,  or  from  sudden  in- 
crease of  the  aortic  insufficiency,  or  from  extensive  athero- 
matous  degeneration  of  the  aortic  walls.  As  a  result,  the 
veins  of  the  systemic  circulation  become  overloaded,  and 
cyanosis  and  dropsy  occur.  The  pulse  now  becomes  feeble 
and  irregular  upon  the  slightest  exertion,  often  intermitting, 
retaining  the  same  jerking  character. 

At  night,  the  patient  is  compelled  to  assume  the  sitting 
posture,  with  his  head  resting  forward  on  some  firm  support. 
The  oedema  of  the  feet  increases ;  attacks  of  extreme  dys- 
pnoea come  on  after  slight  exertion,  accompanied  by  ex- 
treme cyanosis.  The  face  becomes  puffy  ;  pulsation  of  the 
carotids  increases ;  irregularity  and  intermissions  of  the 
pulse  more  marked ;  general  anaemia  is  developed ;  until 
finally  death  occurs  from  pulmonary  oedema,  or  cerebral 
apoplexy,  cerebral  embolism,  or  from  sudden  syncope. 
The  history  of  this  class  of  cases  is  usually  continuous  and 
progressive  ;  the  disease  may  develop  slowly,  but  it  is  cer- 
tain gradually  or  rapidly  to  progress. 

Sometimes  it  is  hastened  to  a  fatal  termination  by  the 
kidney  changes  which  are  certain  to  occur  in  the  advanced 
stages  of  this  form  of  cardiac  disease. 

PHYSICAL  SiG]srs. — The  physical  signs  of  aortic  regurgi- 


AORTIC   REGURGITATION.  337 

ration  are  readily  appreciated  and  not  difficult  of  recog- 
nition. 

Inspection  shows  an  increased  area  of  apex-beat,  with  dis- 
tinct carotid  pulsation  ;  in  an  advanced  stage  of  the  disease, 
the  apex-impulse  becomes  more  diffused  arid  less  distinct. 

On  palpation,  a  distinct  heaving  impulse  is  felt  over  an 
unnatural  area,  which  often  extends  downward  as  far  as  the 
eighth  rib,  and  to  the  left  of  the  left  nipple. 

Upon  percussion  it  will  be  found  that  the  area  of  the 
precordial  dulness  extends  to  the  left  and  below  the  normal 
area,  and  the  outline  of  the  cardiac  area  is  more  oval  in 
shape  than  normal. 

At  first,  the  increased  area  of  dulness  will  extend  to  the 
left  and  downward,  but  as  dilatation  shall  exceed  the 
hypertrophy,  the  abnormal  area  of  dulness  will  extend  up- 
ward rather  than  downward,  and  the  apex  may  be  carried 
as  high  as  the  axillary  space.  The  superficial  area  of  dul- 
ness is  also  increased  to  the  left. 

On  auscultation  a  murmur  will  be  heard  following  or 
taking  the  place  of  the  second  sound  of  the  heart ;  in  some 
instances,  you  will  hear  the  second  sound  of  the  heart, 
normal  and  distinct,  then  the  murmur  following.  This 
murmur  is  usually  heard  with  greatest  intensity  over  the 
second  intercostal  space  close  to  the  right  edge  of  the 
sternum  ;  it  is  diffused  over  a  large  area.  It  may  be  con- 
ducted to  the  apex  of  the  heart,  or  along  the  sternum  to 
the  xiphoid  cartilage.  Sometimes  it  may  be  heard  at  the 
sides  of  the  chest,  and  along  the  spinal  column.  The  area 
of  diffusion  of  an  aortic  murmur  is  greater  than  that  of  any 
other  cardiac  murmur  ;  there  are  louder  murmurs,  but  their 
area  of  diffusion  is  less. 

Whenever  an  aortic  regurgitant  is  heard,  it  is  always  dias- 
tolic,  and  as  a  rule,  its  point  of  maximum  intensity  is  at 
the  base  of  the  heart.  When  combined  with  aortic  ob- 
struction, which  is  very  common,  there  is  a  distinct  double 
murmur  heard  over  a  large  space,  which  may  have  its  max- 
imum in  the  second  intercostal  space  on  the  right  or  left 
edge  of  the  sternum. 

DIFFERENTIAL  DIAGNOSIS.— Generally,  the  diagnosis  of 
22 


338  DIFFERENTIAL   DIAGNOSIS. 

aortic  regurgitation  is  not  difficult,  for  the  reason  that  it 
rests  almost  exclusively  upon  the  existence  or  non-existence 
of  a  diastolic  murmur.  The  existence  of  cardiac  hypertro- 
phy and  dilatation  also  afford  great  assistance  in  arriving  at 
a  diagnosis. 

An  aortic  regurgitant  murmur  can  be  confounded  with 
only  one  cardiac  murmur,  and  that  is  a  mitral  obstructive 
one.  A  mitral  obstructive  murmur  precedes  the  first  sound 
of  the  heart,  commencing  in  the  period  of  repose.  By  some 
observers  it  is  maintained  that  these  murmurs  are  not 
mitral  obstructive,  but  aortic  regurgitant  murmurs,  which 
come  on  after  the  completion  of  the  sound,  the  leakage  at 
the  aortic  valves  not  taking  place  until  after  the  aortic 
recoil. 

If  the  murmur  is  of  mitral  origin,  there  will  be  no  hyper- 
trophy or  dilatation  of  the  left  ventricle  accompanying  it. 

Whenever,  therefore,  you  have  cardiac  hypertrophy  and 
dilatation  confined  to  the  walls  and  cavity  of  the  left  ventri- 
cle, accompanied  by  a  murmur  which  occurs  after  the  sec- 
ond sound  of  the  heart,  during  the  period  of  repose,  al- 
though that  murmur  may  be  heard  with  as  great  intensity 
at  the  apex  of  the  heart  as  at  the  base  ;  the  fact  of  the  ex- 
istence of  the  hypertrophy  of  the  walls  of  the  left  ventricle 
excludes  mitral  stenosis  and  establishes  the  existence  of 
aortic  regurgitation. 

There  is  still  another  condition  with  which  it  is  possible 
to  confound  aortic  regurgitation  ;  namely,  pericarditis. 

When  pericarditis  is  principally  developed  in  that  portion 
of  the  pericardium  which  lies  directly  over  the  aorta,  a  fric- 
tion-sound may  be  heard  which  very  closely  resembles  an 
aortic  regurgitant  murmur.  Such  a  friction-sound  will 
sometimes  be  heard  over  a  considerable  space,  and  it  may 
be  heard  only  during  the  cardiac  diastole.  The  presence  or 
absence  of  left  ventricular  hypertrophy,  and  the  peculiar 
pulse  which  attends  aortic  regurgitation,  will  be  a  sufficient 
basis  upon  which  to  rest  a  differential  diagnosis. 

PROGNOSIS. — The  prognosis  in  aortic  regurgitation  is  gov- 
erned somewhat  by  the  age  of  the  patient.  When  met  with 
in  middle-aged  persons,  engaged  in  active  pursuits,  the 


AOETIC   EEGURGITATIO]^.  839 

prognosis  is  exceedingly  unfavorable ;  in  very  old  persons, 
it  gives  rise  to  little  inconvenience,  and  is  sometimes  present 
for  a  long  time,  without  giving  rise  to  any  dangerous  or 
very  troublesome  symptoms. 

The  first  elements  of  danger  are,  hypertrophy  of  the  ven- 
tricular walls  of  the  left  ventricle,  and  increased  capacity  of 
the  left  ventricular  cavity,  which  so  augments  the  distend- 
ing force  of  the  arterial  walls,  that  degeneration  of  the  arte- 
rial system  may  take  place,  and  render  the  patient  liable  to 
apoplectic  extravasation. 

The  next  element  of  danger  is,  degeneration  of  the  hyper- 
trophied  ventricular  walls,  as  a  result  of  impaired  nutrition 
from  the  interference  of  the  coronary  circulation.  This  de- 
generation allows  of  excessive  dilatation  of  the  ventricular 
cavity,  so  that  the  weakened  ventricle  is  unable  to  overcome 
the  resistance  offered  to  the  circulation  by  the  regurgitation  ; 
as  a  result  we  have  cyanosis  and  dropsy,  which  lead  slowly 
but  surely  to  a  fatal  termination.  These  are  two  prominent 
elements  of  danger  constantly  present  in  a  patient  who  has 
aortic  regurgitation. 

Death  may  also  occur  from  cerebral  embolism.  It  is 
especially  liable  to  occur  with  regurgitation  accompanied 
by  vegetations  on  the  valves,  which  must  always  be  regard- 
ed as  one  of  the  most  serious  and  intractable  forms  of  heart 
disease. 

Another  danger  arises  from  the  obstruction  to  the  sys- 
temic circulation,  giving  rise  to  hardening  of  the  liver  and 
kidneys,  which  interferes  in  a  greater  or  less  degree  with  the 
performance  of  their  functions. 

These  secondary  changes  are  especially  liable  to  occur  in 
connection  with  aortic  regurgitation,  after  there  has  been 
added  to  it  mitral  regurgitation. 

In  all  respects,  aortic  regurgitation  must  be  regarded  as 
one  of  the  gravest  forms  of  cardiac  disease,  and  at  all  times 
necessitates  a  guarded  prognosis. 

A  long  train  of  inevitable  sequences  may  be  predicted 
from  the  very  commencement  of  this  lesion. 


LECTURE    XXIX. 


VALVULAR  DISEASES. 

Aortic  Regurgitation. — Mitral  Obstruction. — Mitral  Regurgitation. 

AT  my  last  lecture,  I  gave  the  history  of  aortic  obstruction 
aud  regurgitation,  with  the  exception  of  their  treatment. 

The  rules  which  are  to  govern  you  in  the  management  of 
aortic  regurgitation  are  the  same  as  those  to  be  observed  in 
the  treatment  of  aortic  obstruction. 

In  the  successful  management  of  these  affections  rest  is  of 
the  first  importance.  All  active  physical  exercise  must  be 
avoided  ;  intemperance  in  eating  and  drinking  must  be  ab- 
stained from,  and  the  diet  must  be  .of  the  most  nutritious 
quality,  chiefly  albuminoid  in  character,  and  must  not  be 
taken  at  any  one  time  in  quantities  sufficiently  large  to  pro- 
duce disturbance  of  the  heart's  action. 

All  forms  of  mental  excitement  must  also  be  carefully 
avoided  by  this  class  of  patients ;  they  must  lead  a  quiet 
life,  having  such  control  over  their  passions  and  appetites 
at  all  times  and  under  all  circumstances,  that  the  heart 
shall  not  be  disturbed  in  its  action.  It  is  wonderful  to  what 
an  extent  active  business  men  suffering  from  these  forms  of 
cardiac  disease  are  often  able  to  control  themselves  in  times 
of  greatest  financial  excitement. 

By  observing  these  simple  rules,  persons  with  aortic 
lesions,  obstruction,  and  regurgitation,  may  live  comfortably 
many  years  after  the  valvular  lesions  have  been  developed, 
when  by  disregarding  them  life  would  be  very  much  short- 
ened. 


AOETIC   OBSTKUCTIOlSr.  341 

These  considerations  are  adapted  to  the  management  of 
all  cardiac  diseases,  but  they  are  especially  applicable  to 
the  management  of  aortic  obstruction  and  regurgitation, 
for  it  is  in  connection  with  these  lesions  that  the  patient  is 
especially  liable  to  sudden  cessation  of  the  heart' s  action  and 
to  those  cerebral  lesions  which  I  have  already  mentioned. 

Digitalis  is  a  drug  which  has  been  very  much  employed 
in  the  treatment  of  valvular  diseases  of  the  heart,  but  it 
should  never  be  resorted  to  in  the  treatment  of  aortic  regur- 
gitation while  the  hypertrophy  compensates  for  the  dilata- 
tion ;  as  soon  as  the  heart  becomes  staggered  in  its  action, 
showing  evidences  of  degeneration  of  the  ventricular  walls 
and  loss  of  heart-power  to  carry  on  the  circulation,  then  digi- 
talis will  be  of  service,  and  in  the  majority  of  instances 
under  such  circumstances,  it  is  remarkable  how  much 
relief  can  be  afforded  to  the  heart.  This  remedy  should 
only  be  administered  in  such  doses  as  will  compensate  for 
the  failure  of  heart- power  ;  when  its  administration  is  con- 
tinued for  a  long  time,  or  it  is  given  in  too  large  doses,  it 
ceases  to  have  power  to  control  the  action  of  the  heart,  and 
you  are  robbed  of  one  of  your  most  serviceable  remedies  in 
the  management  of  this  form  of  heart  disease.  The  best 
mode  of  administering  digitalis  is  -by  infusion.  If  symp- 
toms of  imperfect  heart-power  are  present,  especially  if  the 
patient  is  in  an  anaemic  condition,  iron  will  be  of  great  ser- 
vice. 

The  means  to  be  employed  for  the  relief  of  the  dyspnoea, 
dropsy,  and  other  troublesome  symptoms  of  the  advanced 
stages  of  these  valvular  lesions  will  be  mentioned  under  the 
head  of 'the  management  of  mitral  regurgi cations.  There 
are  but  few  remedial  measures  especially  adapted  to  these 
two  forms  of  valvular  lesions  ;  but  in  the  management  of 
them,  it  is  exceedingly  important  that  you  bear  in  mind 
the  ends  to  be  attained  have  reference  to  failure  of  the  gen- 
eral systemic  circulation  in  contradistinction  to  pulmonary 
obstruction,  which  is  so  important  in  the  management  of 
those  valvular  lesions  which  are  next  to  engage  our  atten- 
tion. 

Your  early  recognition  of  aortic  valvular  lesions  and  of 


342  HOKBID   ANATOMY. 

tlie  causes  which  produce  them,  is  of  the  utmost  impor 
tance,  for  it  will  enable  you  to  adopt  those  measures  which 
shall  delay  their  developmen-t.  After  they  are  fully  deve- 
loped, all  means  are  unsatisfactory.  You  may  be  able  to 
afford  relief,  but  the  relief  is  only  temporary.  The  profes- 
sion are  united  in  regarding  aortic  regurgitation  as  one  of 
the  most  serious  and  intractable  forms  of  cardiac  disease. 
The  remedial  measures  to  be  adopted  in  the  management  of 
each  case  will  be  determined  by  the  individual  symptoms. 

MITRAL  OBSTRUCTION  (Stenosis.) 

I  will  next  consider  diseases  of  the  mitral  orifice,  and  I 
shall  first  direct  your  attention  to  the  obstructive  lesions,  or 
mitral  stenosis. 

Stenosis,  or  obstruction  of  the  auriculo-ventricular  open- 
ing of  the  left  heart,  is  due  partially  to  constriction  at  the 
base  of  the  mitral  valves,  and  partially  to  adhesions  of  the 
valve-tips,  or  chordae  tendinese.  It  usually  occurs  as  a 
consequence  of  rheumatic  endocarditis,  rarely  of  atheroma- 
tous  degeneration,  and  is  most  likely  to  occur  in  endocar- 
ditis affecting  young  persons. 

MOKBID  ANATOMY. — When  endocarditis  affects  the  mitral 
valves  (as  has  already  been  shown),  the  new  connective 
formations,  following  a  universal  law,  contract  in  every 
direction,  so  that  the  valves  become  narrower  and  shorter, 
causing  more  or  less  obstruction  to  the  passage  of  blood 
from  the  auricle  into  the  ventricle,  and  at  the  same  time  the 
valves  do  not  completely  close  the  auriculo-ventricular 
orifice,  so  that  more  or  less  blood  regurgitates  from  the 
ventricle  into  the  auricle  during  the  ventricular  systole. 
Under  such  circumstances,  regurgitation  and  obstruction 
may  coexist. 

In  mitral  stenosis  you  have  not  only  thickening  and  con- 
traction of  the  valves,  but  the  edges  of  the  valves  become 
adherent ;  at  the  same  time  the  chordae  tendineae  and  papil- 
lary muscles  become  adherent,  and  a  sort  of  fibrinous  cone 
is  formed,  with  its  base  looking  toward  the  auricle,  and 
its  apex  toward  the  ventricle,  which  terminates  in  a  narrow 
slit-like  orifice,  through  which  it  is  often  almost  impossible 


MITEAL   OBSTRUCTION.  343 

to  pass  the  tip  of  the  little  finger ;  in  the  normal  condition 
the  auriculo  -  ventricular  opening  is  sufficiently  large  to 
admit  the  introduction  of  three  fingers. 

Vegetations  and  calcareous  plates  often  cover  or  develop 
in  the  valves  in  the  form  of  hard,  wart-like  concretions, 
which  also  tend  to  occlude  the  orifice. 

With  mitral  stenosis,  dilatation  and  hypertrophy  of  the 
left  auricle  are  developed  as  a  necessary  result.  This  is  due 
to  over-distention  of  the  auricle,  and  the  increased  labor  it 
is  called  upon  to  perform  to  force  the  blood  through  the 
constricted  opening  into  the  ventricle.  Following  or  ac- 
companying these  auricular  changes,  the  return  blood  is 
obstructed  in  the  pulmonary  veins,  and  they  become  di- 
lated. This  dilatation  is  purely  mechanical.  The  left  ven- 
tricle remains  of  normal  size,  and  its  walls  are  often  thinner 
than  natural. 

The  distention  of  the  pulmonary  veins  produced  by  the 
dilated  and  over-distended  left  auricle,  causes  congestion  of 
the  entire  pulmonic  circulation,  and  this  leads  to  many 
secondary  changes  in  the  lungs  and  bronchial  tubes.  This 
passive  hypersemia  of  the  lungs  leads  to  those  changes  in 
the  lung-tissue  which  I  have  already  described  under  the 
head  of  brown  induration  of  the  lung. 

The  resulting  hypersemic  condition  which  is  present  in 
the  bronchial  mucous  membrane,  manifests  itself  when  very 
intense,  or  suddenly  increased,  by  a  profuse  secretion  of 
mucus,  which  is  accompanied  by  a  profuse  mucous  expec- 
toration termed  bronchorrhcDa. 

When  this  obstructive  pulmonary  hypersemia  is  very  ex- 
cessive, violent  exercise,  or  severe  paroxysms  of  coughing, 
may  cause  rupture  of  some  of  the  pulmonary  blood-vessels 
and  an  extravasation  of  blood  into  the  lung-substance,  and 
we  then  have  a  true  pulmonary  apoplexy ;  the  clots  are 
firm,  and  of  an  almost  black  color.  These  I  have  described 
under  the  head  of  pulmonary  apoplexy. 

If  persons  with  extensive  mitral  stenosis  walk  rapidly 
against  a  strong  wind,  or  subject  themselves  to  violent 
physical  exertion,  pulmonary  congestion  and  oadema  may 
be  suddenly  developed,  and  cause  sudden  death. 


344  ETIOLOGY. 

When  the  mitral  stenosis  is  slight,  the  pulmonary  ob- 
struction will  be  comparatively  slight,  and  will  not  be  at- 
tended by  any  of  these  alarming  phenomena. 

It  is  often  very  difficult  to  determine  the  exact  extent  of 
the  stenosis  unless  you  see  the  patient  immediately  after 
violent  and  prolonged  physical  exertion. 

When  mitral  stenosis  is  extreme,  the  right  auricle  and 
ventricle  become  hypertrophied  and  dilated. 

ETIOLOGY. — The  changes  in  mitral  obstruction,  or  stenosis, 
are  generally  the  result  of  endocarditis,  and  not  dependent 
upon  atheromatous  degeneration.  Stenosis  is  most  fre- 
quently developed  in  young  subjects ;  mitral  lesion  in  the 
child  is  almost  invariably  mitral  stenosis. 

Diseases  at  the  aortic  orifice,  as  has  already  been  shown, 
lead  to,  or  are  the  cause  of,  mitral  disease ;  and  a  mitral 
valvulitis,  the  result  of  the  extension  of  an  endocardia!  in- 
flammation from  the  aortic  orifice,  or  one  that  is  the  result 
of  the  shock  produced  by  the  aortic  regurgitant  current, 
may,  in  rare  instances,  lead  to  mitral  stenosis.  That  is,  all 
the  causes  which  give  rise  to  acute  or  chronic  endocarditis 
are  indirectly  causes  of  mitral  stenosis. 

If  a  rheumatic  endocarditis  occurs  in  a  very  young  child, 
it  is  almost  certain  to  be  followed  by  such  extensive  con- 
tractions of  the  mitral  orifice  as  to  interfere  with  the  pas- 
sage of  blood  from  the  auricle  to  the  ventricle. 

Sometimes  mitral  stenosis  is  of  congenital  origin. 

SYMPTOMS. — Patients  with  mitral  stenosis,  as  a  conse- 
quence of  the  attending  pulmonary  hypersemia,  are  usually 
short  of  breath  upon  slight  exertion.  As  the  vessels  of  the 
bronchi  are  less  affected  by  the  engorgement  than  those  of 
the  air-cells,  bronchial  catarrh  does  not  necessarily  accom- 
pany the  dyspnoea.  This  class  of  patients  are  habitually 
troubled  with  a  dry,  hacking,  unsatisfactory  cough,  often 
mistaken  for  a  purely  nervous  cough,  which  it  very  closely 
resembles ;  it  is  due  to  the  changes  in  the  lung-tissue  al- 
ready described,  and  not  to  a  disturbed  action  of  the  heart. 
With  the  dyspnoea  and  cough,  haemoptysis  frequently  oc- 
curs, but  it  is  rarely  profuse,  and  the  blood  expectorated  is 
always  of  a  dark  color.  Occasionally,  after  violent  exer- 


MITKAL   OBSTEUCTION.  345 

tion,  there  is  a  profuse,  watery,  blood-stained  expectora- 
tion, indicating  the  occurrence  of  pulmonary  congestion 
and  oedema.  Not  unfrequently  this  class  of  patients  enjoy 
tolerably  good  health,— they  look  pale,  and  are  obliged  to 
use  caution  as  regards  exercise  and  excitement,  but  so  long 
as  they  are  careful,  they  suffer  little  inconvenience.  The 
pulse  is  always  regular  ;  this  is  explained  by  the  fact,  that 
the  ventricle  remains  unaffected  unless  it  be  slightly  dimin- 
ished in  size,  then  it  is  competent  to  discharge  all  the  blood 
which  it  receives  with  its  normal  regularity,  hence  the  reg- 
ularity of  the  pulse. 

When  the  stenosis  is  extensive,  the  pulse  necessarily  be- 
comes feeble,  for  the  reason  that  the  ventricle  does  not  re- 
ceive the  normal  supply  of  blood  at  each  cardiac  pulsation ; 
even  under  excitement  or  violent  physical  exertion,  the 
force  of  the  heart' s  action  is  not  increased. 

Dyspnoea,  cough,  occasionally  bloody  expectoration,  and 
feeble  but  regular  pulse,  are  the  general  symptoms  which 
mark  the  existence  of  mitral  stenosis. 

Cardiac  palpitation  may  be  developed,  especially  after 
exercise,  but  as  soon  as  the  patient  takes  a  recumbent 
posture,  lying  on  the  right  side  with  the  head  slightly  ele- 
vated, the  palpitation  will  cease  ;  by  assuming  this  position 
the  auricle  has  an  opportunity  to  empty  itself,  and  thus 
the  highest  possible  degree  of  equalized  circulation  is  re- 
stored, and  the  palpitation  ceases. 

There  is  one  essential  difference  between  the  pulmonary 
hypersemia  associated  with  mitral  stenosis,  and  that  asso- 
ciated with  mitral  regurgitation ;  the  pulmonary  hyper- 
semia of  mitral  stenosis  is  not  constant,  even  in  cases  well 
advanced,  for  at  times  the  auricle  has  an  opportunity  to 
almost  empty  itself, — but  with  mitral  regurgitation  there  is 
a  constant  driving-back  current  of  blood,  and  the  force  with 
which  it  is  driven  back  corresponds  with  the  force  of  the  ven- 
tricular contractions.  This  brings  us  to  the  consideration 
of  its  physical  signs, — it  is  upon  these  that  you  will  be 
compelled  almost  exclusively  to  rest  for  a  correct  diagnosis. 

PHYSICAL  SIGXS. — Inspection  shows  a  feebler  cardiac  im- 
pulse than  is  natural. 


346  PHYSICAL  SIGNS. 

On  palpation  it  will  be  noticed  that  although  the  apex- 
beat  lacks  force,  yet  there  is  a  distinct  purring  thrill  com- 
municated to  the  hand  as  it  rests  over  the  apex-beat, — this 
thrill  is  a  constant  attendant  of  mitral  stenosis,  and  may 
be  regarded  as  its  diagnostic  sign, — it  precedes  the  full  apex- 
beat,  ceasing  abruptly  as  the  beat  commences. 

A  purring  thrill  is  always  present  in  mitral  stenosis  ;  per- 
haps it  may  occur  without  stenosis,  but  mitral  stenosis 
without  a  purring  thrill  I  have  never  seen. 

Upon  percussion,  an  increased  area  of  dulness  may  be 
found  upward  and  toward  the  left,  in  the  direction  of  the 
left  auricle.  This  will  not  be  easily  recognized,  and  is 
therefore  of  not  so  much  importance. 

On  auscultation,  a  loud  blubbering  murmur  is  heard 
just  preceding  the  first  sound  of  the  heart, — this  murmur 
ends  with  the  commencement  of  the  first  sound  and  the 
apex-beat,  and  is  simultaneous  with  the  contraction  of  the 
auricle.  As  it  takes  a  long  time  for  sufficient  blood  to  pass 
through  the  constricted  auriculo- ventricular  opening  to  fill 
the  ventricle,  this  murmur  is  of  longer  duration  than  any 
other  cardiac  murmur. 

This  murmur  is  heard  with  its  maximum  of  intensity  a 
little  above  the  apex-beat ;  it  is  limited  to  a  circumscribed 
space  around  the  apex. 

In  most  instances,  it  is  heard  over  the  whole  superficial 
cardiac  region  ;  it  is  never  conveyed  to  the  left  of  the  apex, 
nor  heard  behind.  It  varies  in  intensity  with  the  size  and 
character  of  the  obstruction,  the  condition  of  the  blood, 
and  with  the  rapidity  and  force  of  the  blood-current ;  it  is 
usually  louder  than  any  other  cardiac  murmur. 

DIFFERENTIAL  DIAGNOSIS. — The  diagnosis  of  mitral  ste- 
nosis is  not  difficult ;  it  mainly  depends  upon  two  physical 
signs,  the  presence  of  a  murmur,  and  a  purring  thrill.  The 
only  question  which  may  arise  is,  can  this  murmur  be  con- 
founded with  any  other  cardiac  murmur  ?  There  is  no 
other  presystolic  murmur  except  that  which  occurs  at  the 
tricuspid  orifice,  and  that  is  of  such  infrequent  occurrence 
that  it  may  be  thrown  out  of  practical  consideration.  An 
aortic  regurgitant  murmur  sometimes  very  closely  resem- 


MITRAL   OBSTRUCTION.  347 

bles  this  murmur  ;  but  the  murmur  of  mitral  stenosis  is 
presystolic  rather  than  diastolic.  It  is  true  that  an  aortic 
regurgitant  murmur  sometimes  continues  through  the 
period  of  repose  up  to  the  commencement  of  the  first  sound 
of  the  heart ;  but  such  murmurs  are  not  loud,  their  area  of 
diifusion  is  along  the  sternum,  and  their  maximum  of  in- 
tensity is  at  the  base  of  the  heart.  Besides,  aortic  regur- 
gitant murmurs  are  accompanied  by  more  or  less  cardiac 
hypertrophy ;  whereas  mitral  stenosis  never  gives  rise  to 
hypertrophy  of  the  left  ventricle.  The  pulse  of  aortic 
regurgitation  is  irregular  and  jerking ;  while  the  pulse  of 
mitral  stenosis  is  always  regular,  though  it  may  be  feeble. 
Pulmonary  complications  are  always  present  in  mitral 
stenosis,  and  rarely  present  in  aortic  regurgitation.  These 
distinctions,  it  seems  to  me,  are  always  sufficient  to  make  a 
differential  diagnosis  between  these  two  murmurs.  The  time 
of  a  mitral  obstructive  murmur  distinguishes  it  from  a  mitral 
regurgitant. 

PROGNOSIS. — Mitral  stenosis  admits  of  no  compensation ; 
the  pulmonary  hypersemia  which  necessarily  attends  the 
obstruction  to  the  passage  of  blood  from  the  auricle  to  the 
ventricle,  necessarily  induces  more  or  less  parenchymatous 
changes  in  the  lung-substance.  During  violent  physical  ex- 
ercise, such  persons  are  liable  to  sudden  pulmonary  conges- 
tion, oedema,  and  extravasation,  which  may  place  them  in 
a  condition  of  immediate  danger.  When  mitral  stenosis  is 
extensive,  the  danger  attending  it  must  be  ranked  next  to 
that  attending  aortic  regurgitation.  According  to  statistics 
furnished  by  Bellevue  Hospital,  sudden  deaths  occur  as 
frequently  in  connection  with  mitral  stenosis  as  with  aortic 
regurgitation.  When  dyspnoea  is  not  present,  the  prog- 
nosis is  not  very  bad  ;  but  when  constant  dyspnoea  is  pres- 
ent, which  becomes  extreme  upon  active  physical  exertion, 
accompanied  by  occasional  spittings  of  blood,  the  patient 
is  in  very  great  danger. 

There  is  a  class  of  congenital  cases  of  mitral  stenosis ; 
those  belonging  to  this  class  suffer  very  little,  and  are  not 
exposed  to  any  danger  from  it. 

TREATMENT.— The    treatment    of   mitral    obstruction  is 


348  MORBID   ANATOMY. 

nearly  the  same  as  that  of  mitral  regurgitation.  I  shall 
therefore  consider  the  treatment  of  the  two  lesions  undei 
one  head. 

MITRAL  REGURGITATION. 

In  insufficiency  of  the  mitral  valves,  there  is  a  greater 
variety  of  anatomical  changes  than  in  any  other  valvular 
lesion.  In  many  instances  these  changes  are  similar  in  their 
origin  to  those  which  give  rise  to  insufficiency  of  the  aortic 
valves ;  in  other  cases  they  depend  upon  lesions  of  the 
papillary  muscles  and  the  chordae  tendinese. 

As  a  rule,  all  these  changes  are  the  result  of  acute  chronic 
endocarditis.  Mitral  regurgitation  is  more  common  than 
any  other  valvular  lesion,  especially  is  this  the  case  among 
the  young. 

MORBID  ANATOMY. — The  most  common  lesion  which  gives 
rise  to  mitral  regurgitation  is  thickening,  induration,  and 
shortening  of  the  mitral  valves,  the  result  of  the  anatomical 
changes  of  acute  and  chronic  endocarditis. 

Often  large  masses  of  calcareous  matter  are  imbedded  in 
the  indurated  and  thickened  valves.  With  these  valvular 
changes,  the  chordae  tendinese  are  thickened  and  shortened, 
and  the  papillary  muscles  are  diminished  in  bulk. 

In  other  cases,  instead  of  these  lesions,  or  in  connection 
with  them,  the  valves  are  ruptured  or  torn,  or  the  chordae 
tendineae  are  ruptured,  so  that  the  regurgitant  current  of 
blood  causes  them  to  flap  back  through  the  auriculo-ventric- 
ular  opening  into  the  auricle ;  in  rare  instances  the  valves 
become  adherent  to  the  ventricular  walls,  in  consequence  of 
shortenings  produced  in  the  chordae  tendineae,  which  have 
drawn  their  two  surfaces  together,  and  thus  the  valves  are 
prevented  from  approaching  each  other  and  closing  the 
auriculo-ventricular  orifice. 

Again,  there  are  cases  in  which  mitral  regurgitation  exists, 
in  which  no  lesion  can  be  found  sufficient  to  render  the 
valves  insufficient.  In  these  cases  the  valves  and  their 
attachments  are  apparently  perfect,  but  upon  trial  with  the 
water-test,  they  will  be  found  insufficient.  The  only  change 
ascribed  to  this  class  of  cases  is  some  change  in  the  papil- 


MITEAL  KEGUKGITATION".  349 

lary  muscle,  which  penults  the  valves  to  pass  a  trifle  be- 
yond their  normal  limits. 

In  general  terms,  the  valvular  lesions  developed  at  the 
mitral  orifice,  in  mitral  regurgitation,  are  similar  to  those 
described  as  occurring  at  the  aortic  orifice  in  aortic  regurgi- 
tation ;  but,  besides  these  valvular  changes  in  mitral  in- 
sufficiency, there  are  the  other  changes  just  described,  which 
always  have  much  to  do  in  rendering  the  mitral  valves 
insufficient. 

The  first  effect  of  mitral  regurgitation  is  the  same  as  that 
which  is  produced  by  mitral  stenosis  ;  the  cavity  of  the  left 
auricle  becomes  distended,  and  its  walls  are  thickened ; 
consequent  upon  this,  the  pulmonary  circulation  becomes 
distended,  and  the  constant  interference  with  the  return 
circulation  from  the  lungs  interferes  more  or  less  with  the 
outward  current  of  blood  to  the  lungs  from  the  right  ven- 
tricle. As  the  obstruction  is  a  gradual  one,  the  right  ven- 
tricle becomes  so  hypertrophied  as  to  overcome  it,  conse- 
quently the  hypertrophied  right  ventricle  compensates  for 
the  mitral  regurgitation.  So  long  as  the  hypertrophied 
right  ventricle  is  capable  of  compensating  fully  for  the 
abnormal  pressure  of  the  blood  in  the  lungs  from  the  mitral 
regurgitation,  so  long  these  patients  remain  very  comfort- 
able ;  but  a  time  comes,  if  the  mitral  regurgitation  is  con- 
tinued or  increased,  when  the  right  heart  can  no  longer 
compensate  for  the  pressure  upon  the  pulmonary  circula- 
tion, and  then  we  have  dilatation  of  the  right  ventricle 
supervening  upon  its  hypertrophy. 

Consequent  upon  this  dilated  condition  of  the  hyper- 
trophied right  ventricle,  the  return  of  blood  from  the  right 
ventricle  is  necessarily  interfered  with,  and  this  interference 
produces  obstruction  to  the  return  systemic  circulation. 
The  interference  with  the  return  systemic  circulation  man- 
ifests itself  by  more  or  less  cyanosis  upon  exercise,  and  a 
hypersemic  condition  of  all  the  other  organs  of  the  body. 

The  liver,  as  the  result  of  the  constant  hepatic  hyperse- 
niia  produced  by  the  obstruction  to  the  emptying  of  the 
hepatic  vein,  becomes  enlarged  and  hardened  ;  as  a  result  of 
the  interference  to  the  emptying  of  the  hepatic  vein,  the 


350  MORBID   ANATOMY. 

portal  circulation  is  obstructed,  and  we  have,  as  a  result, 
constant  hypergemia  of  the  mucous  membrane  of  the  stom- 
ach and  intestines,  which  necessarily  leads  to  a  disturb- 
ance of  their  functions.  Besides  these  changes,  the  blood, 
as  it  returns  from  the  brain,  finds  an  obstruction  in  an  over- 
distended  auricle,  passive  cerebral  hypersemia  is  the  result, 
and  the  patient  suffers  more  or  less  from  headache  and 
vertigo.  Therefore  it  will  be  seen  that  when  a  patient  has 
reached  the  advanced  stage  of  mitral  regurgitation,  when 
the  right  heart  can  no  longer  compensate  for  the  mitral 
regurgitation,  the  functions  of  all  the  body  are  more  or  less 
disturbed,  and  fluid  accumulates  in  the  areolar  tissue  and 
in  the  cavities,  as  a  result  of  an  imperfectly  maintained 
capillary  circulation.  In  addition  to  the  changes  already 
referred  to,  as  the  result  of  insufficiency  of  the  mitral 
valves,  more  or  less  dilatation  and  hypertrophy  of  the  left 
ventricle  occurs.  These  changes  in  the  left  ventricle  are  pro- 
duced in  this  manner :  during  the  systole  of  the  ventricle, 
the  left  auricle  and  pulmonary  vein  are  over-distended  with 
blood,  which,  as  soon  as  the  ventricular  diastole  occurs, 
rushes  with  abnormal  force  into  the  ventricle,  and  over- 
distends  it  during  its  diastole.  This  over-distension  during 
the  ventricular  diastole  leads  to  dilatation  of  its  cavity,  and 
to  compensate  for  this  dilatation,  as  in  aortic  regurgitation, 
we  have  hypertrophy  of  the  ventricular  walls.  Now,  if 
this  hypertrophy  and  dilatation  of  the  left  ventricle  becomes 
excessive,  the  force  and  volume  of  the  regurgitant  current 
is  increased,  and  under  these  circumstances,  during  physi- 
cal or  mental  excitement,  when  the  activity  of  the  heart  is 
increased,  there  is  great  danger  from  pulmonary  congestion, 
oedema,  and  apoplexy. 


LECTURE  XXX. 


VALVULAR  DISEASES. 

Mitral  Eegurgitation. — Valvular  Diseases  of  the  Right  Heart.— Pulmonic 
Obstruction. — Pulmonic  Regurgitation. 

I  SHALL  this  morning  continue  the  history  of  valvular 
diseases  of  the  heart,  and  their  relations  to  cardiac  mur- 
murs. I  closed  my  last  lecture  with  the  history  of  the  ana- 
tomical lesions  which  attend  the  development  of  mitral  re- 
gurgitation.  I  will  now  say  a  few  words  concerning  their 
etiology,  and  then  pass  to  the  symptoms  which  attend  their 
development. 

ETIOLOGY. — Acute  endocarditis  is  the  primary  cause  of 
most  of  the  changes  which  take  place  at  the  mitral  orifice, 
which  lead  to  mitral  insufficiency.  The  chronic  changes 
which  ordinarily  follow  it,  add  to  the  primary  lesion,  and 
give  rise  to  more  extensive  valvular  changes.  Cases  are 
occasionally  met  with  which  did  not  begin  with  acute  en- 
docarditis, but  in  which  the  endocardial  changes  were 
chronic  from  the  commencement.  Mitral  regurgitation  is 
frequently  secondary  to  lesions  of  the  aortic  valves,  and  is 
produced  in  one  of  the  ways  already  referred  to  ;  either 
from  extension  of  the  endocardial  inflammation  from  the 
aortic  orifice  to  the  mitral  valves  and  their  appendages,  or 
from  chronic  valvulitis  excited  by  the  regurgitant  current 
from  the  aorta.  Mitral  insufficiency  may  be  the  result  of 
the  enlargement  of  the  left  auriculo- ventricular  orifice,  which 
accompanies  excessive  dilatation  of  the  left  ventricle. 

SYMPTOMS.— Patients  during  the  early  stage  of  mitral 


COLLIE  lit  Olr   OSTlEOl-'AT 

l-K\  SIC  1/UvS    k    i  U  KGl£C 


352  SYMPTOMS. 

regnrgitation  suffer  very  little  from  dyspnoea,  so  long  as 
the  compensating  hypertrophy  of  the  right  ventricle  is 
sufficient  to  overcome  the  obstruction  in  the  pulmonary 
circulation.  When  this  compensating  hypertrophy  of  the 
right  ventricle  is  unequal  to  the  task  imposed  upon  it, 
the  systemic  as  well  as  the  pulmonary  circulation  is  im- 
peded, the  veins  and  capillaries  become  overloaded  with 
blood,  the  lips,  face  and  hands  assume  a  bluish  hue,  and 
the  circulation  in  the  brain,  liver,  and  kidneys  becomes  em- 
barrassed. As  the  result  of  the  chronic  hypenemia,  the  liver 
enlarges,  and  patients  complain  of  a  sense  of  weight  and 
fulness  in  the  right  hypochondrium.  This  enlargement  of 
the  liver  is  easily  recognized  by  palpation  and  percussion. 
Sometimes  the  hepatic  circulation  becomes  so  obstructed 
that  the  biliary  secretion  is  interfered  with,  and  a  jaundiced 
hue  of  the  surface  will  be  added  to  the  cyanotic  discolora- 
tion. Cerebral  hypersemia  from  obstructed  venous  return 
may  also  give  rise  to  headache,  vertigo,  stupor,  and  some- 
times to  a  peculiar  form  of  temporary  delirium. 

Gastric  and  intestinal  catarrhs  are  of  quite  frequent  oc- 
currence in  connection  with  extensive  mitral  regurgitation, 
which  causes  obstruction  to  the  gastric  and  intestinal  veins. 
Hemorrhoids  and  menstrual  derangements  occur  from  a 
similar  cause. 

The  obstruction  offered  to  the  return  circulation  of  the 
kidneys,  gives  rise  to  derangements  in  their  functions  ;  the 
urine  may  become  scanty,  high-colored,  and  contain  casts. 
One  of  the  most  constant  symptoms  of  advanced  mitral  re- 
gurgitation  is  dropsy.  The  impoverished  condition  of  the 
blood  from  impaired  nutrition,  and  its  impeded  outflow 
from  the  veins  and  capillaries,  causes  its  watery  portion  to 
exude  through  the  walls  of  the  vessels.  The  dropsy  usu- 
ally begins  in  the  region  of  the  ankles,  and  gradually  ex- 
tends over  the  whole  body.  In  some  cases,  after  the  first 
appearance  of  oedema  about  the  ankles,  the  downward 
course  is  rapid  ;  in  other  cases,  the  downward  progress  is 
slow,  many  years  elapsing  after  its  first  appearance  before 
argent  symptoms  develop. 

When  patients  with  mitral  regurgitation  reach  a  condi- 


MITRAL   REGURGITATION.  358 

tion  of  general  anasarca,  dyspnoea  becomes  extreme,  serous 
effusion  takes  place  into  the  pleura!  and  peritoneal  cavities, 
the  lungs  become  cedematous,  and  these,  with  the  feeble 
and  irregular  heart-action,  are  the  immediate  cause  of. 
death.  In  some  cases,  hemorrhagic  infarctions,  with  thd 
consequent  pneumonic  inflammation,  are  the  direct  causes 
of  the  fatal  termination.  The  pulse  of  mitral  regurgitation 
is  peculiar  and  somewhat  characteristic.  It  is  irregular  i  ; 
volume,  for  with  each  cardiac  pulsation,  less  than  the  noi- 
mal  blood  is  forced  into  the  aorta,  and  this  causes  irregu- 
larity in  the  radial  pulse. 

In  the  later  stages,  the  radial  pulse  becomes  irregular  in 
time  as  well  as  irregular  in  force.  At  one  time  it  is  exceed 
ingly  feeble,  at  another  time  full  but  compressible, 
always  tremulous  when  the  heart's  action  is  much  excited. 
It  is  never  jerking  in  character.  A  cough  with  a  watery 
expectoration  is  usually  present  in  all  advanced  cases  of 
mitral  regurgitation.  The  expectoration  may  be  stained 
with  dark  or  blackish  blood  ;  profuse  hemorrhages  are 
rarely  met  with  in  mitral  insufficiency. 

PHYSICAL  SIGNS. — The  physical  signs,  indicating  the 
existence  of  mitral  insufficiency,  are  generally  very  well 
marked. 

Upon  inspection  and  palpation,  you  will  notice  that  the 
area  of  the  cardiac  impulse  is  increased.  The  visible  im- 
pulse extends  over  more  than  the  normal  area  ;  sometimes  it 
is  very  forcible,  at  other  times  it  is  diffused,  depending  en- 
tirely upon  the  amount  of  hypertrophy  and  dilatation 
which  may  be  present  in  any  given  case. 

The  apex  impulse  is  farther  to  the  left  than  normal ;  when- 
ever the  hypertrophy  predominates,  it  will  be  lower  than 
normal,  while  if  dilatation  predominates,  the  apex-beat  will 
be  higher  than  the  normal  line. 

Upon  percussion,  the  area  of  precordial  dulness  will  be  in- 
creased, extending  to  the  left  beyond  the  normal  precordial 
limits.  The  deep-seated  dulness  may  extend  beyond  the 
left  nipple  and  downward,  indicating  the  existence  of  more 
or  less  hypertrophy  and  dilatation.  The  area  of  the  super- 
ficial dulness  will  also  be  increased  laterally  and  downward. 

23 


354  PHYSICAL   SIGKS. 

Upon  auscultation,  a  murmur  will  be  heard  taking  the 
place  of,  or  following,  the  first  sound  of  the  heart,  ending 
somewhere  between  the  commencement  of  the  first  and  sec- 
ond sounds  of  the  heart.  This  murmur  is  synchronous  with 
the  contracting  and  emptying  of  the  ventricles,  and  is  pro- 
duced by  the  regurgitation  of  the  current  of  blood  from  the 
left  ventricle  into  the  left  auricle.  The  regurgitant  current 
may  be  due  to  any  of  the  changes  at  the  mitral  orifice  which 
I  have  just  described  as  producing  insufficiency  at  the  mitral 
orifice. 

This  murmur  is  heard  with  its  maximum  of  intensity  at 
the  apex-beat ;  its  area  of  diffusion  is  to  the  left,  on  a  line 
corresponding  to  the  apex-beat,  and  is  heard  with  very 
nearly  the  same  intensity  behind,  between  the  lower  border 
of  the  fifth  and  upper  border  of  the  eighth  vertebrae,  close 
to  the  left  side  of  the  spinal  column. 

This  is  characteristic  of  the  murmur  developed  in  connec- 
tion with  mitral  regurgitation.  It  varies  in  quality  in  dif- 
ferent cases,  but  the  quality  of  the  murmur  is  of  little 
practical  importance.  The  point  of  its  maximum  intensity 
is  the  feature  of  special  importance. 

At  the  junction  of  the  third  rib  with  the  sternum  on  the 
left  side,  both  heart-sounds  are  feeble,  but  a  little  above  the 
third  rib,  over  the  pulmonic  valves,  the  second  sound  is  ab- 
normally intense ;  the  increase  in  intensity  of  the  second 
sound  at  this  point  is  often  of  great  diagnostic  value. 

Stenosis  and  regurgitation  at  the  mitral  orifice  are  fre- 
quently met  with  in  the  same  individual.  In  such  a  case 
you  will  have  a  murmur  commencing  before,  and  taking 
the  place  of,  the  first  sound  of  the  heart.  Consequently,  it 
is  a  continuous  murmur,  which  begins  before  the  ventricular 
systole  and  continues  until  the  second  sound  of  the  heart ; 
but  the  presystolic  portion  of  the  murmur  will  not  be  con- 
veyed to  the  left,  and  will  end  with  the  apex-beat.  Fol- 
lowing this,  there  comes  another  murmur,  which  is  the 
regurgitant  murmur,  and  that  will  be  conveyed  around  to 
the  left.  It  is  very  easy  to  draw  the  line  of  distinction  be- 
tween the  two,  although  they  are  mingled  in  a  continuous 
murmur.  It  is  quite  important  to  recognize  the  fact,  when 


MITEAL   REGURGITATION.  355 

stenosis  exists  with  a  mitral  regurgitation,  for  when  stenosis 
is  present,  you  are  more  liable  to  have  pulmonary  congestion 
suddenly  developed,  and  its  presence  will  consequently 
modify  the  prognosis  in  any  given  case. 

DIFFERENTIAL  DIAGNOSIS.  —  Usually  the  diagnosis  of 
mitral  regurgitation  is  not  difficult.  The  seat  and  rhythm 
of  the  murmur  and  its  area  of  diffusion  are  generally  suffi- 
cient to  enable  you  to  distinguish  a  mitral  regurgitant  mur- 
mur from  any  other. 

Again,  the  character  of  the  pulse  will  be  of  assistance. 
The  pulse  of  mitral  regurgitation  is  feeble  and  easily  accel- 
erated, differing  in  these  respects  from  the  hard,  jerking 
pulse  of  aortic  regurgitation. 

A  mitral  regurgitant  murmur  occurring  with  the  first 
sound  of  the  heart  may  be  mistaken  for  an  aortic  obstruc- 
tive or  tricuspid  regurgitant  murmur.  An  aortic  obstructive 
murmur  is,  however,  rarely  heard  as  low  in  the  chest  as  the 
mitral  regurgitant ;  and  it  is  conveyed  along  the  course  of 
the  arteries  instead  of  being  transmitted  to  the  left  of  the 
apex  and  backward. 

A  tricuspid  regurgitant  murmur,  although  heard  with  the 
first  sound  of  the  heart,  is  not  conveyed  to  the  left  of  the 
apex-beat,  but  is  heard  with  greatest  intensity  directly  over 
the  right  ventricle,  and  if  transmitted  in  any  direction  will 
be  conveyed  to  the  right.  In  addition  to  these  distinguish- 
ing features,  we  have  the  pulmonary  hypersemia  incident  to 
mitral  disease,  which  is  not  present  in  connection  with  aortic 
and  tricuspid.  These  facts,  properly  considered  and  intel- 
ligently applied,  will  be  sufficient  to  enable  you  to  make  a 
correct  diagnosis  in  nearly  every  instance. 

PROGNOSIS. — The  prognosis  in  mitral  regurgitation,  as  far 
as  duration  of  life  is  concerned,  is  good.  It  is  a  lesion  of 
the  heart  which  does  not  rapidly  undergo  changes.  The 
valvular  lesions  which  produce  it  are  of  slow  growth,  and 
their  tendency  is  to  remain  stationary ;  besides,  valvular 
insufficiency  at  the  mitral  orifice  admits  of  compensation 
more  than  any  other  valvular  lesion. 

Patients  with  a  moderate  regurgitation  at  the  mitral  ori- 
fice suffer  very  little  except  after  taking  violent  exercise, 


356  DIFFEKEXTIAL   DIAGNOSIS. 

when  dyspnoea  may  be  developed  to  a  slight  degree,  and 
were  it  not  for  this  inconvenience,  it  would  hardly  be  known 
that  they  were  the  subjects  of  cardiac  disease. 

So  long  as  the  compensating  hypertrophy  of  the  right 
ventricle  is  sufficient  to  overcome  the  obstruction  to  the 
pulmonary  circulation,  patients  with  this  form  of  cardiac 
disease  may  experience  no  difficulty  of  breathing,  even 
after  violent  physical  exercise. 

Mitral  regurgitation  uncomplicated  by  any  other  valvular 
lesion  gives  rise  to  very  little  disturbance  of  the  systemic 
capillary  circulation. 

It  may  exist  for  years  without  inducing  either  general 
dropsy  or  systemic  congestion. 

Patients  will  live  longer  and  enjoy  a  more  comfortable 
degree  of  health  with  mitral  regurgitation  than  with  any 
other  extensive  valvular  lesion.  It  is  for  this  reason  that 
many  persons  having  this  form  of  cardiac  disease  are  igno- 
rant of  its  existence.  Do  not  disturb  the  equanimity  of 
such  individuals  by  gravely  saying  to  them  that  they  have 
heart  disease ;  such  knowledge  may  be  productive  of  the 
most  serious  results,  for  the  patient  is  not  able  to  appreci- 
ate the  difference  between  cardiac  lesions.  With  one  form 
of  cardiac  lesion  the  patient  may  live  for  years  in  compara- 
tive comfort ;  while  with  another,  he  may  live  only  a  short 
time,  and  a  statement  from  his  medical  adviser  that  he  has 
heart  disease  will  necessarily  direct  his  attention  constantly 
to  the  heart,  and  so  tend  to  hasten  the  development  of  the 
unpleasant  and  dangerous  features  of  this  form  of  cardiac 
lesion. 

Whenever  there  are  evidences  of  interference  with  the 
systemic  circulation,  we  may  know  that  the  right  side  of 
the  heart  is  not  able  to  overcome  the  pulmonary  obstruc- 
tion ;  this  is  shown  by  the  occurrence  of  oedema,  cyanosis,  ex- 
treme dyspnoea,  etc.,  and  the  prognosis  is  very  unfavorable. 

When  these  symptoms  have  developed,  the  result  only 
becomes  a  question  of  time.  You  may  relieve  your  patient, 
but  the  beginning  of  the  end  has  commenced  ;  until  these 
evidences  of  the  failure  of  heart-power  are  present,  the  prog- 
nosis is  not  immediately  unfavorable. 


MITRAL   EEGURGITATIOlSr.  357 

TREATMENT. — Although  you  cannot  hope  by  the  adop- 
tion of  any  special  therapeutical  measures  to  effect  a  cure 
in  any  case  of  valvular  disease,  and  although  you  may  not 
be  able  by  any  medicinal  agents  to  prevent  to  any  great 
extent  the  cardiac  hypertrophy  and  dilatation  which  neces- 
sarily accompanies  it,  yet  there  is  much  to  be  accomplish- 
ed by  the  judicious  medicinal  and  hygienic  treatment  of  all 
valvular  disease,  and  especially  of  mitral  regurgitation. 

It  is  important  that  a  patient  with  mitral  insufficiency 
should  lead  a  quiet  life,  free  from  all  excitement,  and  in 
this  respect  should  follow  the  same  general  directions  which 
were  given  for  patients  with  aortic  insufficiency,  but  not  for 
the  same  reasons,  for  the  dangers  of  the  two  conditions  are 
not  the  same. 

Avoidance  of  excitement  and  absolute  self-control  are  not 
the  only  important  things  in  the  management  of  a  patient 
who  is  suffering  from  mitral  regurgitation. 

The  most  troublesome  feature  of  these  cases  is  the  ob- 
struction to  the  pulmonary  circulation,  hence  anything  and 
everything  which  has  a  tendency  to  increase  this  obstruc- 
tion must  be  avoided.  If  the  patient's  occupation  is  such  as 
compels  him  to  breathe  an  atmosphere  which  predisposes  to 
the  development  of  pulmonary  hypersemia,  or  catarrh  of 
the  bronchi,  a  change  of  occupation  should  at  once  be 
made. 

The  use  of  the  voice,  either  in  singing  or  speaking,  until 
dyspnoea  is  produced,  is  exceedingly  prejudicial  to  this 
class  of  patients,  and  should  be  forbidden.  The  pulmonary 
hypersemia  which  attends  mitral  regurgitation,  I  stated  to 
you  was  constant ;  but  you  are  not  warranted  in  taking  any 
active  measures  for  its  relief  unless  it  has  reached  a  point 
at  which  pulmonary  oedema  occurs.  Then  it  is  a  question 
whether  the  administration  of  a  hydragogue  cathartic,  or 
even  moderate  blood-letting  may  not  be  of  service ;  but 
these  measures  are  never  to  be  resorted  to  unless  the 
oedema  is  excessive.  Under  any  circumstances,  you  are 
not  warranted  in  resorting  to  those  measures  which  are 
usually  classed  under  the  head  of  antiphlogistics.  As  in 
certain  conditions  which  are  present  in  the  other  valvular 


358  TKEATMENT. 

diseases  which  have  just  engaged  our  attention,  the  two 
remedies  which  will  be  found  to  furnish  the  most  satis- 
factory results  are  digitalis  and  iron. 

By  the  judicious  use  of  digitalis  you  will  not  only  relieve 
the  pulmonary  hypersemia,  but  you  will  also  relieve  the 
systemic  circulation.  The  immediate  effect  of  the  admin- 
istration of  this  drug  is  to  regulate  and  increase  the  force 
of  the  heart' s  systole,  and  this  is  accomplished  by  the  tonic 
effect  of  the  digitalis  on  the  cardiac  muscle  ;  it  strengthens 
the  right  heart,  and  enables  the  left  ventricle  to  resist  the 
increasing  dilatation  of  its  cavity.  When  dropsy  is  present, 
digitalis  acts  as  a  diuretic  by  adjusting  the  renal  circula- 
tion, and  thus  permitting  a  larger  amount  of  blood  to  flow 
through  the  renal  vessels.  In  ordinary  cases,  it  is  not 
necessary  that  the  patient  should  take  digitalis  continually. 
In  its  administration  the  aim  should  be  to  employ  only 
such  doses  as  will  equalize  the  circulation.  As  soon  as  the 
circulation  has  been  restored  to  its  equilibrium,  and  has 
been  maintained  for  twenty -four  or  forty-eight  hours,  the 
digitalis  should  be  discontinued,  at  least  for  a  time,  for  this 
reason,  that  a  time  will  come  sooner  or  later  in  the  progress 
of  the  case,  when  the  digitalis  will  cease  to  have  any  tonic 
effect  upon  the  heart,  and  the  longer  that  period  can  be 
postponed,  the  more  benefit  will  be  derived  from  its  use. 
When  judiciously  administered,  and  the  patient  is  not  per- 
mitted to  become  accustomed  to  its  use,  it  is  one  of  the 
most  serviceable  and  reliable  remedies  that  can  be  employed 
in  the  treatment  of  this  form  of  cardiac  disease.  At  times, 
when  the  mitral  disease  has  been  far  advanced,  I  have  seen 
pulmonary  osdema,  cyanosis,  anasarca,  and  hepatic  en- 
largements disappear,  the  urine,  which  had  been  scanty, 
become  abundant,  and  the  patient,  from  a  condition  of  ex- 
treme suffering  and  apparently  near  death,  pass  into  a 
condition  of  comparative  comfort  within  twenty-four  or 
forty-eight  hours  after  the  administration  of  the  digitalis. 
Large  doses  of  digitalis  are  sometimes  required  to  accom- 
plish the  desired  result ;  half  an  ounce  of  the  infusion  every 
two  hours  for  twenty-four  hours  is  sometimes  necessary  to 
fully  control  the  heart's  action.  The  relief  obtained  by  its 


MITRAL  EEGUKGITATIOK.  359 

administration  is  in  a  certain  proportion  of  cases  per- 
manent. 

Whenever  the  digitalis  fails  to  restore  the  muscular 
power  of  the  heart,  and  compensate  for  the  degenerative 
changes  which  it  has  undergone,  it  ceases  to  be  of  service 
and  may  be  harmful. 

When  we  find  a  case  in  the  treatment  of  which  digitalis 
has  never  been  employed,  we  may  be  sure  that  we  can  at 
least  restore  the  patient  to  a  state  of  comparative  comfort 
by  its  administration. 

When  iron  is  administered  to  patients  with  mitral  insuf- 
ficiency, it  should  always  be  given  in  connection  with  the 
food,  and  is  better  to  give  it  in  full  doses. 

Again,  when  the  patient  is  not  in  an  ansemic  condition, 
iron  is  never  to  be  administered,  as  it  produces  a  sensation 
of  fulness  about  the  head.  Usually  the  patient  is  not 
ansemic  in  the  earlier  stages  of  the  disease,  but  becomes  so 
as  the  disease  advances.  Anaemia  is  more  common  in  fe- 
males than  in  males,  consequently  they  require  a  free  and 
prolonged  use  of  some  preparation  of  iron.  Vallet's  mass 
may  frequently  be  administered  with  marked  benefit  in 
doses  of  ten  to  twenty  grains  three  times  a  day.  The 
hygienic  management  of  patients  with  this  disease  will  be 
similar  to  that  of  patients  suffering  from  other  cardiac  af- 
fections. 

VALVULAR  DISEASES   OF  THE  RIGHT  HEART. 

I  will  now  briefly  consider  valvular  diseases  of  the  right 
heart,  and  their  relations  to  cardiac  murmurs. 

The  majority  of  the  valvular  diseases  met  with  on  the 
right  side  of  the  heart  are  secondary  to  diseases  of  the  left 
side  ;  consequently,  they  are  not  of  equal  importance  with 
those  of  the  left  heart.  So  infrequent  are  valvular  diseases 
of  the  right  heart,  that  when  the  unqualified  term  valvular 
disease  is  used,  it  is  always  understood  to  mean  that  of  the 
left  heart.  The  reason  for  the  infrequency  of  valvular 
lesions  upon  the  right  side  of  the  heart  is  to  be  found  in 
the  fact  that  endocarditis  rarely  occurs  upon  this  side,  ex- 
cept during  intra-uterine  life  ;  atheroma  of  the  pulmonary 


360  PULMONIC   OBSTRUCTION. 

artery  and  valves  is  equally  rare ;  consequently,  valvulai 
deformities  which  usually  originate  in  one  of  these  marked 
processes  have  been  met  with  in  few  instances. 

Whenever  valvular  deformities  do  occur  upon  the  right 
heart,  the  same  morbid  changes  are  present  that  have  been 
described  as  giving  rise  to  similar  changes  in  the  left  heart. 
It  is  unnecessary  for  me  to  minutely  describe  these  ana- 
tomical changes. 

When  endocarditis  occurs  upon  the  right  side  of  the 
heart,  it  is  usually  confined  to  the  tricuspid  valves ;  the 
reason  for  this  is  to  be  found  in  the  fact  that  these  valves 
are  more  especially  subjected  to  the  tension  that  is  pro- 
duced in  the  right  side  of  the  heart,  in  consequence  of  the 
obstruction  to  the  pulmonic  circulation  produced  by  dis- 
ease of  the  left  heart,  especially  of  the  mitral  valves.  This 
valvular  tension  excites  an  inflammation  of  the  endocar- 
dium of  the  tricuspid  valves,  and  as  a  result  of  that  in- 
flammation, similar  valvular  changes  take  place  in  the 
tricuspid  valves  as  have  already  been  described  as  taking 
place  in  the  mitral  valves  when  they  are  the  seat  of  endo- 
carditis. 

DISEASES  OF  THE  PULMONIC  VALVES. — I  will  first  direct 
your  attention  to  the  changes  which  may  occur  in  the  pul- 
monic valves  and  at  the  pulmonic  orifice. 

On  account  of  the  infrequency  of  diseases  of  the  pul- 
monic valves,  very  little  is  known  of  the  phenomena  to 
which  such  diseases  may  give  rise.  In  fact,  they  are  so 
rare,  and  as  we  have  no  written  history  of  their  objective 
symptoms,  their  diagnosis  is  arrived  at  chiefly  by  exclusion. 
They  can  only  be  recognized  during  life  by  the  physical  signs 
which  attend  them — all  the  objective  symptoms  admitting 
of  a  two-fold  interpretation. 

PULMONIC  OBSTRUCTION,  or  stenosis,  gives  rise  to  a  mur- 
mur which  is  heard  with  the  first  sound  of  the  heart,  having 
its  maximum  of  intensity  directly  over  the  seat  of  the  pulmo- 
nic valves  ;  it  is  very  superficial  and  consequently  very  dis- 
tinct ;  it  is  limited  in  its  diffusion,  being  inaudible  at  the 
apex  of  the  heart,  or  along  the  sternum  ;  it  is  never  heard 


PULMONIC   BEGURGITATION.  361 

in  the  neck,  nor  along  the  course  of  the  aorta  ;  il  it  has  an 
area  of  diffusion  it  is  toward  the  left  shoulder. 

I  have  never  heard  but  two  pulmonic  obstructive  mur- 
murs where  subsequent  autopsies  were  obtained ;  in  both 
cases  it  was  found  that  the  murmur  had  been  produced, 
not  by  any  change  at  the  pulmonic  orifice,  but  by  a  medi- 
astinal  tumor  pressing  on  the  pulmonic  artery,  so  as  to  di- 
minish its  calibre,  and  thus  cause  an  obstruction  to  the 
current  of  blood. 

PULMONIC  REGURGITATION  is  even  more  rare  than  pul- 
monic obstruction, — some  doubt  its  occurrence. 

Theoretically,  a  murmur  produced  by  regurgitation  at 
the  pulmonic  orifice  should  be  heard  with  the  second  sound 
of  the  heart  ;  its  maximum  of  intensity  should  be  directly 
over  the  pulmonic  valves,  and  its  area  of  diffusion  should 
be  downward  toward  the  xiphoid  cartilage  ;  there  should 
be  no  jerking  character  to  the  pulse,  nor  visible  pulsation 
of  the  superficial  arteries,  which  are  the  constant  attendants 
of  aortic  regurgitati'on,  and  by  the  absence  of  which  you 
would  be  able  to  make  at  least  a  differential  diagnosis. 

As  yet,  I  have  never  heard  such  a  pulmonic  regurgitant 
murmur. 

The  diagnosis  of  stenosis  or  regurgitation  at  the  pulmonic 
orifice  must  necessarily  be  difficult,  and  the  utmost  cau- 
tion must  be  exercised  to  make  it  certain  that  the  maximum 
of  intensity  of  the  murmur  indicating  its  presence,  is  di- 
rectly over  the  pulmonic  orifice,  and  that  a  supposed  pul- 
monic murmur  is  not  conducted  from  the  aorta. 

PROGNOSIS. — Theoretically,  the  prognosis  in  diseases  of 
the  pulmonic  orifice  must  be  exceedingly  bad,  especially 
when  added  to  diseases  of  the  left  side  of  the  heart.  If  it 
should  be  developed  as  a  primary  affection,  its  direct  effect 
on  the  right  ventricle  is  dilatation  of  its  cavity  and  the 
development  of  tricuspid  regurgitation.  If  at  all  extensive, 
it  must  lead  to  the  gravest  results,  for  the  amount  of  blood 
sent  to  the  lungs  with  each  cardiac  impulse  would  be  dimin- 
ished, and  a  constant  disturbance  to  the  systemic  circula- 
tion would  be  the  result.  If  excessive  dilatation  and  hy- 


362  TEEATHENT. 

pertrophy  should  occur  as  the  result,  it  would  become  one 
of  the  gravest  of  heart  diseases. 

TBEATMEXT. — The  treatment  must  be  expectant,  and  you 
should  be  guided  by  the  same  general  rules  as  those  which 
govern  you  in  the  management  of  mitral  lesions,  as  the  pri- 
mary disturbance  will  be  in  the  pulmonary  circulation. 


LECTURE    XXXI. 


VALVULAE  DISEASES  AND  VALVULAR 
MURMURS. 


Tricuspid  Stenosis. — Tricuspid  Regurgitation. — Diagnosis  of  Cardiac 

Murmurs. 

I  WILL  continue  the  history  of  valvular  diseases,  and  theix 
relation  to  valvular  murmurs,  by  inviting  your  attention  to 
diseases  at  the  tricuspid  orifice.  The  valves  at  this  orifice 
are  much  more  frequentlythe  seat  of  disease  than  is  usually 
supposed  ;  tricuspid  regurgitation  hastens  the  fatal  issue  in 
very  many  patients  with  chronic  cardiac  disease. 

Obstruction,  or  stenosis,  at  the  tricuspid  orifice  is  of  so 
rare  occurrence,  that  there  are  no  established  rules  for  its 
diagnosis. 

Theoretically,  it  should  give  rise  to  a  presystolic  murmur, 
having  its  point  of  maximum  intensity  at  the  base  of  the 
ensiform  cartilage,  and  it  should  be  accompanied  by  very 
intense  general  venous  congestion  (cyanosis).  On  these 
data  some  have  rested  a  diagnosis  which  was  not  con- 
firmed by  a  post-mortem  examination. 

Tricuspid  stenosis  is  a  lesion  which  I  have  never  seen. 

TRICUSPID  REGURGITATION. 

Regurgitation  at  the  tricuspid  orifice  is  not  an  infrequent 
valvular  lesion, — primary  disease  of  the  tricuspid  valves 
is,  however,  of  rare  occurrence. 


364  MORBID   ANATOMY. 

In  nearly  every  instance  tricuspid  disease  is  secondary  to 
stenosis  or  regurgitation  at  the  mitral  orifice. 

MORBID  ANATOMY. — The  valvular  lesions  which  lead  to 
tricuspid  insufficiency  are  similar  to  those  which  produce 
mitral  insufficiency.  There  is  thickening  and  shrinking  of 
the  valvular  apparatus,  the  chordae  tendinese  are  shortened, 
and  the  valves  are  sometimes  adherent  to  the  ventricles  ; 
besides,  there  is  more  or  less  thickening  and  induration  at  the 
base  of  the  valves,  which  somewhat  diminishes  the  size  of 
the  auriculo-ventricular  orifice.  Vegetations  and  athero- 
matous  changes  are  rarely  met  with  at  the  tricuspid  orifice  ; 
the  changes  are  almost  entirely  those  of  chronic  endocar- 
ditis. 

The  first  effect  of  this  lesion  is  to  cause  dilatation  of  the 
right  auricle  ;  following  this  dilatation  there  will  be  more  or 
less  hypertrophy  of  its  walls. 

Just  here  is  an  interesting  anatomical  fact.  The  veins 
which  empty  into  the  right  auricle,  coming  from  the  upper 
part  of  the  body,  are  provided  with  valves,  while  those  which 
convey  the  blood  to  the  right  auricle  from  below,  are  not 
provided  with  valves  ;  consequently,  while  the  valves  of  the 
veins  from  the  upper  part  of  the  body  remain  intact,  the 
distention  and  entire  force  of  the  regurgitation  is  first  ex- 
pended upon  the  hepatic  veins  ;  as  a  result,  the  primary  pres- 
sure from  tricuspid  regurgitation  is  felt  by  the  liver,  and 
this  organ  is  the  first  whose  function  is  interfered  with.  The 
constant  mechanical  hypersemia  increases  the  size  of  the  or- 
gan, and  with  its  enlargement  a  certain  dingy  hue  of  the 
skin  is  almost  always  present. 

The  valves  in  the  veins  which  return  the  blood  from  the 
upper  part  of  the  body,  will  for  a  time  prevent  the  regurgi- 
tant  current  from  interfering  with  the  systemic  circulation 
of  that  portion  of  the  body  from  which  they  derive  their 
supply  of  blood.  After  a  time,  however,  these  valves  be- 
come insufficient,  and  the  consequence  is  that  the  jugular 
veins,  and  the  veins  of  the  neck,  head,  and  upper  extremi- 
ties, become  distended,  which  distention  interferes  with  the 
systemic  circulation  of  the  upper  part  of  the  body. 

With  extreme  dilatation  of  the  right  auricle  from  exten- 


TRICUSPID   REGURGITATION.  365 

sive  tricuspid  regurgitation,  and  the  consequent  interference 
with  the  return  circulation  of  the  body,  the  left  ventricle  be- 
comes secondarily  involved  because  of  the  increased  amount 
of  labor  it  has  to  perform.  Under  such  circumstances  the 
primary  lesion  is  upon  the  right  side  of  the  heart,  and  the 
secondary  lesion  is  upon  the  left ;  but  in  a  majority  of  cases 
the  primary  lesion  is  upon  the  left  side  of  the  heart,  and  the 
secondary  lesion  upon  the  right  side. 

ETIOLOGY. — Primary  tricuspid  regurgitation  is  of  doubt- 
ful occurrence.  It  may  occur  as  the  result  of  an  interfer- 
ence with  the  pulmonary  circulation,  such  as  may  be  devel- 
oped in  connection  with  pulmonary  emphysema.  Under 
the  influence  of  this  condition  of  the  lungs,  or  any  other  in 
which  the  pulmonary  circulation  becomes  impeded,  the  right 
heart  becomes  over-distended,  and  there  is  an  abnormal 
stress  thrown  on  the  valves  and  valvular  attachments  at  the 
tricuspid  opening,  which  leads  to  the  development  of 
endocardial  inflammation  at  those  points  where  the  stress 
is  most  severe,  and  from  this  endocarditis  the  valvular 
changes  already  referred  to  are  developed. 

When  tricuspid  disease  is  developed  in  connection  with 
mitral  disease,  some  have  attributed  its  development  to  sym- 
pathy of  the  right  side  of  the  heart  with  a  diseased  condi- 
tion of  the  left  heart.  By  far  the  more  probable  explanation 
of  the  development  of  tricuspid  disease  under  such  circum- 
stances, is  the  one  I  have  already  given,  that  an  abnormal 
stress  is  thrown  upon  the  right  heart  by  the  interference 
with  the  pulmonic  circulation.  This  is  produced  by  the  re- 
gurgitant  current  at  the  mitral  orifice,  which  leads  to  endo- 
cardial inflammation  of  the  right  heart. 

SYMPTOMS. — The  symptoms  during  the  early  stage  of  tri- 
cuspid regurgitation  are  vague,  and  by  no  means  diagnostic. 
Occurring  as  it  does  in  the  great  majority  of  instances  in 
connection  with  mitral  disease,  any  special  cardiac  phe- 
nomena which  may  attend  it,  are  liable  to  be  marked  by  the 
symptoms  which  attend  the  mitral  disease.  As  soon,  how- 
ever, as  the  regurgitant  pressure  through  the  tricuspid  ori- 
fice interferes  materially  with  the  venous  return,  such  inter- 
ference is  shown  by  disturbances  in  the  function  of  those 


366  SYMPTOMS. 

organs  whose  venous  circulation  is  most  obstructed.  The 
liver  gives  evidence  of  a  tricuspid  regurgitation  by  a  uniform 
enlargement  of  the  organ,  and  by  a  dinginess  of  the  surface 
of  the  body ;  the  kidneys  by  scanty  urine,  and  the  other 
phenomena  of  Bright' s  disease;  the  brain  by  headache, 
vertigo,  and  by  peculiar  mental  disturbances  which  are  not 
met  with  in  any  other  form  of  cardiac  disease. 

You  will  also  notice  that  as  soon  as  the  valves  of  the 
jugular  veins  are  no  longer  able  to  prevent  the  regurgitant 
current  from  flowing  in  that  direction,  a  pulsation  in  these 
veins  will  attend  each  cardiac  pulsation ;  perhaps  this  is 
the  most  characteristic  symptom  of  tricuspid  regurgitation. 
Now,  if  you  place  the  patient  in  a  horizontal  position,  with 
his  head  on  the  same  plane  as  the  rest  of  the  body,  in  a  few 
moments  his  face  will  become  blue  and  turgid  ;  and  if  you 
retain  him  in  this  position  any  length  of  time,  stupor  and 
coma,  with  the  other  alarming  symptoms  of  cerebral  oppres 
sion,  will  follow. 

The  presence  of  these  symptoms  in  one  who  has  long  suf- 
fered from  mitral  disease,  or  who  is  the  subject  of  advanced 
pulmonary  emphysema,  or  any  other  chronic  pulmonary 
disease  that  is  attended  with  extensive  obstruction  to  the 
pulmonary  circulation,  should  lead  to  the  suspicion  of  tri- 
cuspid regurgitation.  The  positive  existence  or  non-exist- 
ence of  tricuspid  regurgitation  may  generally  be  determined 
by  a  careful  physical  examination,  although  its  physical 
signs  are  by  no  means  as  distinctive  as  the  other  valvular 
lesions  which  we  have  been  considering. 

PHYSICAL  SIGJSTS. — Inspection  will  show  an  increase  in 
the  area  of  the  visible  cardiac  impulse,  extending  some- 
times from  the  apex-beat  to  the  xiphoid  cartilage,  and  at 
times  it  will  be  conveyed  even  as  high  as  the  right  second 
intercostal  space.  A  more  extensive  area  of  impulse  is  met 
with  in  extensive  tricuspid  regurgitation  than  with  any 
other  valvular  lesion.  This  extended  cardiac  impulse  is 
generally  accompanied  by  a  visible  pulsation  in  the  dis- 
tended jugular  veins. 

This  jugular  pulsation  may  ~be  regarded  as  a  charac- 
teristic symptom  of  tricuspid  regurgitation. 


TEICTJSPID   REGURGITATIOlSr.  367 

Upon  palpation,  unless  there  is  considerable  hypertrophy 
of  the  left  ventricle,  there  will  be  an  indistinct  apex-beat. 
You  will  also  notice  a  distinct  epigastric  pulsation.  The 
explanation  of  this  pulsation  lies  in  the  fact  that  the  hyper- 
trophied  and  dilated  right  ventricle  rests  more  than  nor- 
mally upon  that  portion  of  the  diaphragm  which  lies  in  con- 
tact with  the  left  lobe  of  the  liver,  and  through  that  organ 
the  pulsation  is  communicated  to  the  abdominal  parietes. 

Epigastric  pulsation  may  occur  under  other  circumstances, 
but  it  is  always  present  when  tricuspid  regurgitation  has 
reached  a  point  at  which  jugular  pulsation  is  developed. 

Upon  percussion,  the  area  of  dulness  will  be  found  to  be 
abnormally  increased  to  the  right  of  the  sternum,  and  up- 
ward as  high  as  the  second  intercostal  space. 

On  auscultation,  a  distinct  blowing  murmur  is  heard 
with,  or  taking  the  place  of  the  first  sound  of  the  heart. 
This  murmur  is  superficial  in  character,  rarely  audible 
above  the  third  rib,  and  on  this  account  readily  distin- 
guished from  aortic  and  pulmonic  murmurs ;  its  point  of 
maximum  intensity  is  between  the  fourth  and  sixth  ribs, 
along  the  left  border  of  the  sternum.  When  there  is  ex- 
tensive hypertrophy  and  dilatation  of  the  right  side  of  the 
heart,  the  point  of  maximum  intensity  of  the  murmur  is  at 
the  junction  of  the  fourth  rib  with  the  sternum.  It  is 
rarely  if  ever  heard  to  the  left  of  the  apex-beat.  There  is  a 
marked  increase  in  the  intensity  of  the  second  sound  of  the 
heart  over  the  pulmonic  valve. 

With  extensive  tricuspid  regurgitation  there  is  an  irregu- 
larity in  the  action  of  the  heart,  accompanied  by  cardiac  pal- 
pitation and  severe  attacks  of  cardiac  dyspnoea  ;  these,  com- 
bined with  jugular  pulsation,  render  the  diagnosis  easy  and 
certain. 

DIFFERENTIAL  DIAGNOSIS.— The  diagnosis  of  tricuspid 
regurgitation  mainly  rests  upon  the  presence  of  the  mur- 
mur produced  by  the  regurgitation.  There  are  three  other 
murmurs  which  may  occur  at  the  same  period  in  the  heart's 
action,  which  may  necessitate  a  diagnosis  between  them 
and  a  murmur  of  tricuspid  regurgitation.  These  three  are 
aortic  obstructive,  the  pulmonic  obstructive,  and  the  mitral 


368  DIFFERENTIAL   DIAGNOSIS. 

regurgitant,  all  of  which  occur  with  the  first  sound  of  the 
heart. 

The  mitral  regurgitant  murmur  is  heard  with  the  first 
sound  of  the  heart,  but  the  murmur  is  conveyed  around  to 
the  left  of  the  apex-beat,  and  is  heard  behind ;  while  the 
tricuspid  regurgitant  murmur,  although  it  is  heard  with 
the  same  sound  of  the  heart,  has  its  area  of  diffusion  to  the 
right. 

Again,  tricuspid  regurgitation  is  distinguished  from  pul- 
monic  obstruction  by  the  fact  that  the  murmur  accompany- 
ing it  is  not  heard  above  the  third  rib.  For  the  same  rea- 
son it  can  easily  be  distinguished  from  aortic  obstruction ; 
besides,  an  aortic  obstructive  murmur  is  heard  along  the 
vessels  of  the  neck,  while  the  tricuspid  regurgitant  is  not. 

In  addition  to  these  distinctions,  when  the  tricuspid  re- 
gurgitation  is  advanced,  you  will  have  the  epigastric  im- 
pulse, also  the  jugular  pulsation,  and  the  cerebral  dis- 
turbances already  referred  to.  These,  taken  in  connection 
with  the  seat  and  area  of  diffusion  of  the  murmur  which 
accompanies  it,  will  enable  you  in  nearly  every  instance  to 
make  a  positive  diagnosis. 

PROGNOSIS. — When  tricuspid  regurgitation  is  added  to  a 
valvular  lesion  on  the  left  side  of  the  heart,  the  prognosis 
is  very  unfavorable.  In  primary  tricuspid  regurgitation, 
such  as  is  developed  in  connection  with  pulmonary  emphy- 
sema, the  prognosis  is  also  bad,  especially  when  the  tricus- 
pid insufficiency  has  reached  a  point  where  epigastric  and 
jugular  pulsation  are  present.  In  this  class  of  cases,  the 
veins  rapidly  yield  to  the  regurgitant  distending  force, 
which  gives  rise  to  the  changes  in  the  systemic  circula- 
tion, to  which  reference  has  already  been  made. 

TREATMENT. — With  regard  to  the  treatment  of  tricuspid 
regurgitation,  the  same  hygienic  rules  are  to  be  observed 
which  have  been  given  in  connection  with  the  other  cardiac 
lesions.  The  patient  must  lead  a  quiet  life,  and  he  is  usu- 
ally better  in  a  warm  climate,  where  a  free  action  of  the 
skin  can  be  more  readily  maintained.  The  administration 
of  heart  tonics  is  only  admissible  when  the  tricuspid  regur- 
gitation is  accompanied  by  extensive  mitral  regurgitation. 


TEICUSPID   EEGUEGITATIOlSr.  369 

When  it  occurs  in  connection  with  pulmonary  emphysema, 
it  has  been  found  that  digitalis  is  not  well  borne,  for  the 
reason  that  it  increases  jugular  pulsation,  and  has  a  ten- 
dency to  increase  the  distention  of  the  veins  of  the  head  and 
neck. 

When  this  lesion  accompanies  mitral  regurgitation,  espe- 
cially if  disturbance  of  the  systemic  circulation  has  com- 
menced, the  administration  of  digitalis  is  generally  service- 
able. 

Iron  may  also  be  administered  according  to  the  rules 
already  given.  Drastic  cathartics  will  temporarily  relieve 
the  venous  engorgement  and  the  cerebral  oppression  which 
results  from  the  obstruction  of  the  return  current  from  the 
brain  ;  but  the  relief  is  only  temporary,  and  when  general 
anasarca  is  developed,  incision  or  needle-pricking  of  the 
most  oedematous  parts  is  the  only  way  to  relieve  the  patient. 
These  measures  will  be  more  fully  considered  in  another 
connection.  This  completes  the  direct  history  of  the  valvu- 
lar lesions  of  the  heart. 

Before  leaving  this  subject,  however,  I  will  review  in  a 
summary  manner  the  diagnostic  features  of  cardiac  mur- 
murs. I  will  glance  at  the  entire  class  of  cardiac  murmurs, 
and  shall  endeavor  to  fix  your  attention  upon  some  impor- 
tant practical  points. 

DIAGNOSIS  OF  CAEDIAC  MUEMUES. — By  the  term  cardiac 
murmur  is  meant  a  sound  produced  by  some  obstruction  to 
the  current  of  blood  ;  or  one  produced  by  an  abnormal  di- 
rection to  the  current  of  blood,  or  by  some  change  in  the 
blood  itself. 

You  have  already  recognized  the  fact  that  it  is  not  the 
loudest  nor  the  roughest  murmur  that  is  the  most  impor- 
tant. The  existence  of  a  cardiac  murmur  does  not  necessa- 
rily indicate  extensive  disease  of  the  heart,  nor  that  there  is 
any  immediate  or  remote  danger  attending  the  case. 

In  any  case,  as  soon  as  you  recognize  the  existence  of  a 
cardiac  murmur,  first  determine  its  rhythm ;  then  its  seat 
and  area  of  diffusion.  By  the  rhythm  of  a  murmur  is  meant 
its  relation  to  the  sound  of  the  heart.  This  can  only  be  de- 
termined by  a  careful  stethoscopic  examination.  Before 

24 


370  DIAGNOSIS. 

entering  upon  this  examination,  let  us  for  a  moment  care- 
fully study  the  manner  in  which  you  are  to  determine  which 
is  the  first  and  which  is  the  second  sound  of  the  heart. 

You  are  already  aware  that  the  production  of  the  first 
sound  of  the  heart  is  synchronous,  or  nearly  synchronous 
with  certain  external  manifestations.  As,  for  instance,  with 
the  first  sound  of  the  heart  a  pulsation  may  be  felt  in  the 
neck  ;  and  soon  after,  the  same  pulsation  may  be  felt  in  the 
radial  artery.  The  apex-beat  and  the  radial  pulse  are  the 
two  most  reliable  and  easily  appreciated  external  phenomena 
indicating  the  occurrence  of  the  cardiac  systole  and  the  pro- 
duction of  the  first  sound  of  the  heart. 

In  this  way  the  first  sound  is  easily  determined  when  the 
heart  is  beating  slowly,  but  it  may  be  very  difficult  to  rec- 
ognize it  when  the  action  of  the  heart  is  rapid.  If  a  mur- 
mur takes  place  with  the  first  sound  of  the  heart,  it  will 
bear  the  same  relation  to  the  radial  pulse  and  the  apex-beat 
that  the  first  sound  does. 

Again,  the  second  sound  of  the  heart  may  be  recognized 
by  certain  characteristics.  It  is  a  short,  sharp  sound,  and 
may  always  be  heard,  for  both  pulmonic  and  aortic  valves 
will  never  be  involved  in  disease  at  the  same  time.  The 
loudest  aortic  murmur  will  not  destroy  the  second  sound  to 
such  an  extent  that  the  pulmonic  element  of  the  second 
sound  cannot  be  heard.  In  order  that  you  may  more  fully 
appreciate  the  relations  of  the  sounds  to  the  physiological 
acts  attending  a  cardiac  pulsation,  I  will  follow  the  course 
of  the  blood  through  the  heart,  commencing  with  the  left 
auricle.  As  it  contracts  at  the  end  of  the  period  of  repose,  a 
small  quantity  of  blood  is  forced  from  it  through  the  mitral 
orifice  into  the  already  very  nearly  filled  left  ventricle,  but 
in  the  normal  heart  no  sound  is  produced  by  its  passage. 
As  soon  as  the  left  ventricle  becomes  distended  with  the 
blood  forced  into  it  by  the  auricular  systole,  a  ventricular 
contraction  immediately  follows.  As  soon  as  the  ven- 
tricular contraction  commences,  the  mitral  and  tricuspid 
valves  are  closed,  and  the  aortic  and  pulmonic  valves  are 
opened. 

With  the  contraction  of  the  left  ventricle,  the  blood  is 


CAKDIAC   MUEMUES.  371 

propelled  with  considerable  force  into  the  aorta,  and  pass- 
ing through  the  systemic  circulation,  is  returned  by  the 
veins  to  the  right  auricle  ;  from  the  right  auricle  it  passes 
through  the  tricuspid  orifice  into  the  right  ventricle.  The 
right  ventricle  contracts  synchronously  with  the  left  ventri- 
cle, the  tricuspid  valves  close,  the  pulmonic  valves  open,  and 
the  blood  from  the  right  ventricle  is  propelled  into  the  pul- 
monary artery  and  is  returned  by  the  pulmonary  veins  to 
the  left  auricle. 

The  periods  of  activity  and  rest  of  the  two  sides  of  the 
heart  are  simultaneous.  During  the  auricular  systole, 
while  both  auricles  are  contracting  and  expelling  blood,  and 
both  ventricles  are  receiving  and  becoming  distended  with 
blood,  no  sound  is  produced.  During  the  ventricular  sys- 
tole, while  both  ventricles  are  contracting  and  expelling 
blood,  and  both  auricles  are  receiving  and  becoming  dis- 
tended with  blood,  the  first  sound  of  the  heart  is  produced  ; 
immediately  following  the  emptying  of  the  ventricles  the 
second  sound  occurs,  and  then  comes  the  period  of  repose, 
which  lasts  from  the  commencement  of  the  ventricular 
diastole  to  the  commencement  of  the  auricular  systole,  the 
ventricles  remaining  in  a  state  of  perfect  rest,  receiving  but 
not  becoming  distended  with  blood.  During  the  period  of 
rest  no  sound  is  heard. 

Having  then  ascertained  the  existence  of  an  endocardia! 
murmur,  the  first  step  in  your  investigation  is  to  determine 
which  is  the  first,  and  which  is  the  second  sound  of  the 
heart ;  having  done  this,  determine  the  relation  of  the 
murmur  to  these  sounds — for  all  valvular  murmurs  pre- 
cede, take  the  place  of,  or  immediately  follow  one  of  the 
heart-sounds. 

A  murmur  which  precedes  and  ends  with  the  first  sound 
and  the  apex-beat,  is  simultaneous  with  the  contraction  of 
the  auricles,  and  is  either  a  mitral  or  tricuspid  obstructive 
murmur,  and  depends  either  upon  stenosis  of  the  mitral  or 
tricuspid  orifice. 

A  murmur  which  takes  the  place  of,  or  follows  the  first 
sound  of  the  heart,  ending  somewhere  between  the  first  and 
second  sound,  is  coincident  with  the  contraction  and  empty- 


372  DIAGNOSIS. 

ing  of  the  ventricles,  and  must  be  caused  either  by  obstruc- 
tion to  the  current  of  blood  as  it  flows  outward  from  the 
ventricles  in  its  natural  direction  into  the  aorta  and  pul- 
monary artery,  or  backward  by  a  regurgitant  current 
through  the  mitral  or  tricuspid  valves. 

A  murmur  may  take  the  place  of,  or  follow  the  second 
sound,  ending  somewhere  in  the  period  of  repose.  This 
murmur  is  simultaneous  with  the  dilatation  of  the  ven- 
tricles, and  is  produced  by  a  regurgitant  current  through 
the  aortic  or  pulmonary  valves. 

Having  determined  the  relation  of  a  cardiac  murmur  to 
the  sounds  of  the  heart,  the  next  step  is,  by  a  careful 
stethoscopic  examination,  to  determine  the  exact  seat  and 
limits  of  diffusion  of  the  murmur.  If  the  murmur  is  very 
loud  or  diffused,  or  if  there  are  several  murmurs  present, 
this  may  sometimes  be  difficult,  but  in  a  large  majority  of 
cases  you  will  be  able  to  fix  upon  a  few  points,  or  a  few 
restricted  spaces  over  which  each  murmur  is  heard,  or  an 
area  within  which  it  is  heard  with  greatest  intensity. 

As  there  are  four  valvular  orifices  at  which  the  majority 
of  endocardia!  murmurs  are  produced,  so  there  are  four 
distinct  areas  to  which  murmurs  arising  at  these  orifices 
may  be  conveyed. 

Mitral  regurgitant  murmurs  have  their  point  of  maxi- 
mum intensity  a  little  to  the  left  of  the  apex-beat,  and  their 
area  of  diffusion  is  to  the  left  and  backward,  in  a  line  cor- 
responding to  the  apex-beat.  They  are  heard  with  very 
nearly  equal  intensity  behind,  a  little  to  the  left  of  the  ver- 
tebrae, between  the  lower  border  of  the  fifth  and  upper 
border  of  the  eighth  rib,  as  in  front. 

Mitral  obstructive  murmurs  have  their  maximum  of  in- 
tensity a  little  to  the  right  of  the  apex-beat ;  their  area  of 
diffusion  is  limited  to  the  precordial  space.  They  become 
indistinct  as  you  pass  to  the  left  of  the  apex,  and  they  are 
never  heard  behind. 

Tricuspid  murmurs  (obstructive  and  regurgitant)  have 
their  maximum  of  intensity  along  the  margin  of  the  fifth 
and  sixth  costal  cartilages  on  the  left  side ;  their  area  of 
diffusion  corresponds  to  that  portion  of  the  right  ventricle 


CAEDIAC   MURMURS.  873 

which  is  uncovered  by  lung- tissue.  They  are  rarely  heard 
above  the  third  rib,  or  to  the  left  of  the  apex. 

Pulmonic  murmurs  have  their  maximum  of  intensity 
directly  over  the  seat  of  the  valves.  Their  area  of  diffusion 
is  limited  ;  they  are  usually  inaudible  at  the  apex  and 
along  the  lower  portion  of  the  sternum  ;  if  they  are  con- 
veyed in  any  direction,  it  is  toward  the  left  shoulder. 

Aortic  obstructive  murmurs  have  their  maximum  of  in- 
tensity at  the  junction  of  the  second  rib,  with  the  sternum 
on  the  right  side.  Their  area  of  diffusion  is  upward,  along 
the  course  of  the  arteries  into  the  vessels  of  the  neck. 
They  are  usually  inaudible  at  the  apex,  and  are  rarely 
heard  to  the  left  of  the  apex. 

Aortic  regurgitant  murmurs  have  their  maximum  of 
intensity  at  the  junction  of  the  third  rib,  with  the  sternum 
on  the  left  side.  Their  area  of  diffusion  is  downward  along 
the  sternum ;  sometimes  they  are  louder  at  the  xiphoid 
cartilage  than  at  any  other  point. 

To  complete  the  diagnosis  of  endocardial  murmurs,  it  is 
necessary  to  consider  their  rhythm  in  connection  with  the 
apex-beat  and  area  of  diffusion. 

Presystolic  murmurs,  or  those  which  immediately  pre- 
cede the  first  sound  of  the  heart,  may  be  mitral  or  tricuspid 
obstructive.  In  any  case,  the  maximum  of  intensity  of  the 
murmur  will  be  a  little  to  the  right  of  the  apex-beat,  and 
its  area  of  diffusion  will  be  limited  to  the  precordial  space. 

Systolic  murmurs,  or  murmurs  accompanying  or  follow- 
ing the  first  sound  of  the  heart,  may  be  produced  either  in 
the  auriculo-ventricular,  or  in  the  aortic  or  pulmonic  ori- 
fices, and  they  have  four  distinct  solutions. 

First :  If  a  murmur  with,  or  following  the  first  sound  of 
the  heart,  has  its  origin  at  the  mitral  orifice,  it  is  a  mitral 
regurgitant  murmur,  and  its  point  of  maximum  intensity 
will  be  a  little  to  the  left  of  the  apex-beat ;  it  will  be  con- 
veyed to  the  left,  and  heard  behind. 

Second :  If  a  murmur  with,  or  following  the  first  sound 
of  the  heart,  has  its  origin  at  the  tricuspid  orifice,  it  will  be 
a  tricuspid  regurgitant  murmur.  Its  maximum  of  intensity 
will  be  a  little  to  the  right  of  the  apex-beat,  and  its  area  of 


374  DIAGNOSIS. 

diffusion  will  correspond  to  that  portion  of  the  heart  which 
is  uncovered  by  lung-tissue ;  it  may  be  conducted  to  the 
right  of  the  sternum  at  the  junction  of  the  fifth  rib. 

Third  :  If  a  murmur  with,  or  following  the  first  sound  of 
the  heart,  has  its  origin  at  the  aortic  orifice,  it  is  an  aortic 
obstructive  murmur.  Its  point  of  maximum  intensity  will 
be  at  the  right  second  sterno-costal  articulation,  and  it  will 
be  conveyed  into  the  vessels  of  the  neck. 

Fourth :  If  a  murmur  with,  or  following  the  first  sound 
of  the  heart,  has  its  origin  at  the  pulmonic  orifice,  it  will  be 
a  pulmonic  obstructive  murmur.  Its  maximum  of  intensity 
will  be  directly  over  the  pulmonic  valves,  a  little  above  the 
junction  of  the  third  rib  with  the  sternum  on  the  left  side, 
and  its  area  of  diffusion  is  toward  the  left  shoulder. 

Diastolic  murmurs,  or  murmurs  accompanying  or  follow- 
ing the  second  sound  of  the  heart,  may  be  produced  at  the 
aortic  or  pulmonic  orifice.  In  either  case,  they  coincide  with 
the  filling  of  the  ventricles. 

First :  If  a  murmur  accompanying  or  following  the  sec- 
ond sound  of  the  heart  has  its  origin  at  the  aortic  orifice, 
it  is  an  aortic  regurgitant  murmur.  Its  maximum  of  in- 
tensity is  at  the  junction  of  the  third  rib  with  the  sternum 
on  the  right  side,  and  its  area  of  diffusion  is  downward 
along  the  sternum  to  the  xiphoid  cartilage. 

Second :  If  a  murmur  following  the  second  sound  of  the 
heart  has  its  origin  at  the  pulmonic  orifice,  it  is  a  pulmonic 
regurgitant  murmur.  Its  maximum  of  intensity  is  just 
above  the  junction  of  the  third  rib  with  the  sternum  on  the 
left  side,  and  it  is  conveyed  downward  to  the  right  of  the 
apex-beat.  In  some  cases  you  will  have  combined  two  or 
three,  or  even  four,  of  the  murmurs  we  have  been  consid- 
ering. 

The  most  frequent  combinations  are  the  aortic  obstructive 
and  regurgitant ;  next,  the  mitral  obstructive  and  regurgi- 
tant ;  then,  perhaps,  both  the  aortic  and  mitral. 

Murmurs  occurring  on  the  right  side  of  the  heart  are  com- 
paratively of  rare  occurrence ;  the  tricuspid  regurgitant  is 
the  only  one  of  importance. 

Whenever  a  murmur  is  heard  in  the  vessels  of  the  neck, 


CARDIAC  MURMURS.  375 

it  is  either  an  aortic  obstructive  or  an  anaemic  murmur.  If 
anaemic,  it  will  be  heard  with  its  maximum  of  intensity  in 
the  carotids ;  if  an  aortic  obstructive,  it  will  be  heard  with 
greatest  intensity  at  the  junction  of  the  second  rib  with  the 
sternum  on  the  right  side. 

It  is  sometimes  difficult  to  make  a  differential  diagnosis 
between  a  tricuspid  regurgitant  murmur  and  a  pericardial 
friction- sound,  both  sounds  being  heard  with  greatest  inten- 
sity over  that  portion  of  the  right  ventricle  which  is  uncov- 
ered by  lung-tissue. 

A  reference  to  the  rules  I  have  already  given  for  the  dif- 
ferential diagnosis  between  pericardial  friction-sounds  and 
endocardial  murmurs  will  enable  you  to  settle  such  diffi- 
culties. 


LECTURE  XXXII. 


CARDIAC  HYPERTROPHY. 

Definition. — Varieties. 

HAVING  completed  the  history  of  valvular  diseases  of  the 
heart,  and  their  relation  to  valvular  murmurs,  I  will  pass  to 
the  consideration  of  cardiac  hypertrophy.  I  have  already 
referred  to  this  subject  in  connection  with  the  history  of 
valvular  lesions,  but  its  frequent  occurrence,  and  its  very 
great  importance  in  connection  with  the  history  of  all  car- 
diac diseases,  render  it  necessary  that  I  should  enter  into  its 
history  more  in  detail. 

By  the  term  cardiac  hypertrophy  is  meant  thickening  of 
the  walls  of  the  heart  by  an  increase  in  their  muscular  tis- 
sue. This  muscular  increase  may  be  confined  to  one  por- 
tion of  the  heart,  or  it  may  involve  the  walls  of  both  auricles 
and  ventricles. 

There  are  three  recognized  forms  of  cardiac  hypertrophy. 

First. — SIMPLE  HYPERTROPHY. 

In  this  form  there  is  an  increase  in  the  thickness  of  the 
walls  of  the  heart,  but  the  capacity  of  the  cavities  is  not  in- 
creased. Simple  hypertrophy  is  usually  confined  to  the 
left  ventricle,  and  is  most  frequently  met  with  in  connection 
with  chronic  Bright' s  disease  and  chronic  alcoholismus. 

Second. — ECCENTRIC  HYPERTROPHY. 

In  this  form  there  is  thickening  of  the  walls  of  the  heart, 
with  increase  in  the  capacity  of  its  cavities.  It  is  most 
commonly  met  with,  or  occurs  as  the  result  of  some  valvu- 
lar lesion. 

Third. — CONCENTRIC  HYPERTROPHY. 

In  this  form,  there  is  thickening  of  the  walls  of  the  heart, 

ith  diminution  in  the  size  of  the  cavities.     Some  observers 


CAEDIAC   HYPERTEOPHY.  377 

deny  the  occurrence  of  this  form  of  hypertrophy,  and  claim 
that  the  diminution  in  the  capacity  of  the  cavities  is  only 
apparent  —  that  it  is  the  result  of  violent  ventricular  con- 
traction just  prior  to  death.  I  have  never  seen  an  example 
of  this  form  of  hypertrophy,  and  mention  it  only  for  the 
reason  that  your  attention  is  called  to  it  in  most  of  your 
text-books. 

MOEBID  ANATOMY.  —  The  anatomical  changes  which  take 
place  in  cardiac  hypertrophy  vary  according  to  its  seat, 
and  somewhat  according  to  the  character  of  the  hypertro- 


In  eccentric  hypertrophy,  there  will  always  be  an  increase 
in  the  size  of  the  papillary  muscles,  and  the  septum  will  be 
thickened,  which  does  not  necessarily  occur  in  connection 
with  simple  hypertrophy. 

It  is  often  difficult,  even  after  death,  to  determine  the  ex- 
istence of  a  moderate  degree  of  cardiac  hypertrophy  ;  while 
extensive  hypertrophy  is  very  readily  recognized. 

When  cardiac  hypertrophy  exists,  the  first  thing  to  be 
noticed  is  a  change  in  the  shape  of  the  organ,  and  that 
change  will  correspond  to  the  seat  of  the  hypertrophy. 

If  the  hypertrophy  is  confined  to  the  left  ventricle,  either 
simple  or  eccentric,  the  heart  will  assume  a  more  than 
usual  pyriform  shape,  and  will  become  elongated  —  the 
right  ventricle  seems  to  be  a  mere  appendage  to  the  left. 

On  the  other  hand,  hypertrophy  of  the  right  ventricle  in- 
creases the  horizontal  measurement  of  the  organ,  and  gives 
it  a  more  oval  shape. 

If  all  the  cavities  of  the  heart  are  increased  in  capacity, 
and  their  walls  hypertrophied,  the  whole  heart  will  be  in- 
creased in  size,  but  the  change  will  be  most  marked  in  its 
horizontal  direction,  and  the  organ  will  assume  a  globular 
shape. 

In  connection  with  any  form  of  hypertrophy,  it  will  be 
noticed  that  the  cardiac  walls  are  stiff,  so  that  when  the  cav- 
ities are  opened  and  the  blood  has  been  removed  from  them 
they  do  not  collapse. 

The  color  of  the  muscular  tissue  of  a  hypertrophied  heart 
is  redder  than  that  of  normal  cardiac  muscle. 


378  MORBID   ANATOMY. 

Cardiac  hypertrophy  is  really  a  hyperplasia  ;  there  is  an 
increase  in  the  number  of  the  muscular  fibres,  differing  in  no 
way  in  their  anatomical  structure  from  the  normal  heart-mus- 
cular fibre  ;  it  is  simply  an  anatomical  growth  of  the  normal 
tissue  of  the  heart.  There  may  be,  occasionally,  an  increase 
in  the  size  of  the  cardiac  muscular  fibres,  but  the  hyper- 
trophy mostly  consists  in  an  increase  in  their  number. 

There  is  no  particular  limit  to  cardiac  hypertrophy.  The 
heart  may  reach  such  a  degree  of  enlargement  as  to  weigh 
forty  ounces  more  than  when  in  its  normal  state.  After  the 
hypertrophy  reaches  a  certain  point  we  have  dilatation,  and 
preceding  and  accompanying  this  form  of  dilatation  there  is 
fatty  degeneration,  which  first  occurs  in  the  more  recently 
formed  muscular  fibres. 

An  increase  in  the  number  or  size  of  the  muscular  fibres 
of  the  heart-walls,  causes  a  corresponding  increase  in  the 
power  of  the  heart's  action. 

In  general  terms,  cardiac  hypertrophy  is  the  result  of  over- 
work ;  for  some  reason  the  cardiac  walls  are  called  upon  to 
perform  more  than  their  normal  amount  of  labor,  and  an  in- 
crease in  the  number  of  the  muscular  fibres  necessarily  fol- 
lows an  increase  in  the  labor  performed  by  muscular  tissue. 

The  walls  of  a  hypertrophied  heart  vary  in  thickness  ac- 
cording to  the  cause  of  the  hypertrophy.  The  walls  of  the 
left  ventricle  may  become  an  inch  and  a  half,  or  even  two 
inches  in  thickness,  while  those  of  the  right  ventricle  rarely 
reach  an  inch  and  a  half  in  thickness. 

The  heavier  a  heart  becomes,  the  deeper  does  it  lie  in  the 
thoracic  cavity ;  the  diaphragm  is  pushed  down,  and  the 
heart  inclines  more  to  the  left  of  the  thorax. 

ETIOLOGY. — Whenever  the  function  of  the  heart  is  perma- 
nently or  repeatedly  overtaxed,  or  when  the  resistance  which 
it  should  normally  encounter  is  increased,  hypertrophy  of 
its  walls  is  the  result.  The  modes  by  which  it  is  directly 
induced  are  as  follows  : 

First. — Dilatation  of  the  Cavities  of  the  Heart. — Under 
certain  circumstances,  many  of  which  have  already  been  re- 
ferred to,  dilatation  of  one  or  all  of  the  cavities  of  the  heart 
takes  place  during  its  diastole ;  the  capacity  of  the  cavities 


CAKDIAC  HYPEETROPHY.  379 

is  consequently  increased,  and  they  receive  more  than  their 
normal  quantity  of  blood.  A  certain  degree  of  force  is  re- 
quired to  discharge  the  normal  quantity  of  blood  from  the 
heart-cavities  ;  if  there  is  more  than  the  normal  quantity,  a 
greater  than  the  normal  degree  of  force  is  required  to  expel  it. 

This  demand  for  increased  heart-power  is  supplied  by  an 
increase  of  muscular  fibres  in  the  heart- walls, — the  hypertro- 
phy is  developed  in  proportion  to  the  increase  of  force 
required  to  properly  perform  the  increased  amount  of  labor. 
This  is  the  cause  of  those  forms  of  cardiac  hypertrophy 
developed  in  connection  with  valvular  lesions,  which  have 
recently  engaged  our  attention. 

Under  these  circumstances,  the  hypertrophy  is  always 
eccentric,  and  is  not  due  so  much  to  the  valvular  lesions  as 
to  the  dilatation  of  the  heart-cavities  which  occurs  as  the 
result  of  these  lesions. 

The  order  is,  first,  dilatation  ;  then,  hypertrophy,  to  com- 
pensate for  the  dilatation.  The  dilatation  is  developed  dur- 
ing the  cardiac  diastole  ;  the  hypertrophy  during  the  car- 
diac systole. 

Second. — Mechanical  Obstruction. — There  is  a  long  list 
of  mechanical  obstructions  which  will  give  rise  to  cardiac 
hypertrophy. 

The  first  which  I  shall  name  are  those  which  originate 
in  the  heart.  Aortic  stenosis  gives  rise  to  hypertrophy  of 
the  left  ventricle ;  mitral  stenosis,  to  hypertrophy  of  the 
left  auricle  ;  pulmonic  disease,  to  hypertrophy  of  the  right 
ventricle  ;  tricuspid  stenosis,  to  hypertrophy  of  the  right 
auricle.  The  other  valvular  lesions  which  are  attended  by 
cardiac  hypertrophy,  first  cause  dilatation  of  the  heart- cavi- 
ties, and  the  hypertrophy  as  already  shown  develops  as  the 
result  of  the  dilatation. 

Again,  in  this  list  of  mechanical  causes  are  included  all 
those  diseases  of  the  arteries  which  give  rise  to  increase  of 
heart-power.  The  walls  of  the  large  arteries  may  lose  their 
elasticity  from  atheromatous  degeneration,  or  they  may  be 
constricted  or  dilated,  and  thus  offer  obstruction  to  the 
blood-current.  An  aneurismal  tumor  may  have  developed 
sufficiently  to  obstruct  the  current  of  blood,  or  some  tumor 


380  ETIOLOGY. 

may  press  upon  and  diminisli  the  calibre  of  the  aorta ; 
under  such  circumstances,  a  more  than  normal  amount  of 
work  will  be  imposed  upon  the  left  ventricle,  and  simple 
cardiac  hypertrophy  will  be  developed  as  the  result. 

Again,  obstruction  to  the  pulmonary  circulation  will  give 
rise  to  hypertrophy  of  the  wTalls  of  the  right  ventricle ;  in 
many  instances,  dilatation  will  occur  prior  to  the  hypertro- 
phy, but  in  quite  a  large  number  of  cases,  direct  hypertro- 
phy of  the  right  ventricular  walls  will  occur  as  the  result  of 
obstruction  to  the  pulmonary  circulation.  Such  obstruc- 
tion may  be  developed  in  connection  with  pulmonary  em- 
physema, chronic  pleurisy,  and  other  chronic  diseases 
which  interfere  with  the  circulation  of  blood  through  the 
lungs.  It  does  not  ordinarily  occur  in  pulmonary  phthisis, 
for  the  reason  that  the  pulmonary  circulation  is  not  ob- 
structed to  any  great  extent  by  the  phthisical  changes. 

Again,  hypertrophy  of  the  left  ventricle  occurs  as  the 
result  of  interference  with  the  general  capillary  circulation. 
Examples  of  this  are  met  with  in  cases  of  chronic  Bright' s 
disease,  especially  when  the  kidneys  have  undergone  atro- 
phy. Simple  hypertrophy  of  the  cardiac  walls  is  one  of 
the  most  constant  attendants  of  this  stage  of  kidney  disease. 

In  chronic  alcoholismus,  rheumatic  hyperinosis,  or  any 
other  condition  which  interferes  with  the  systemic  capillary 
circulation,  more  or  less  extensive,  simple  cardiac  hypertro- 
phy of  the  left  ventricle  is  developed. 

Anything  which  increases  for  any  length  of  time  the 
rapidity  and  force  of  the  heart' s  contraction,  may  produce 
cardiac  hypertrophy.  Among  this  class  of  causes  may  be 
included  excessive  and  prolonged  muscular  exercise. 

Pericarditis  is  not  unfrequently  a  cause  of  cardiac  hyper- 
trophy, either  by  inducing  softening  and  dilatation  of  the 
ventricles,  or  by  the  obstruction  which  is  offered  to  the 
heart's  action  by  the  adhesions  between  the  two  surfaces 
which  result  from  the  inflammatory  processes. 

You  will  occasionally  meet  with  cases  where  no  cause 
can  be  found  for  the  cardiac  hypertrophy. 

In  detailing  the  causes  of  hypertrophy  of  the  walls  of  the 
heart,  I  have  confined  myself  to  the  primary  hypertrophy. 


CARDIAC   HYPERTROPHY.  381 

In  order  that  you  may  not  be  misled  by  these  statements,  it 
is  well  for  you  to  remember  that  hypertrophy  of  the  walls 
of  one  cavity  is  soon  followed  by  increase  in  the  walls  oi 
other  cavities.  For  instance,  hypertrophy  of  the  left  ven- 
tricle, after  a  time,  leads  to  hypertrophy  of  the  right  ven- 
tricle, and  hypertrophy  of  the  right  ventricle  leads  to  that 
of  the  right  auricle,  and  secondarily  to  that  of  the  left 
ventricle. 

SYMPTOMS. — It  is  exceedingly  difficult  to  exactly  describe 
the  phenomena  which  attend  cardiac  hypertrophy  ;  it  almost 
always  depends  upon,  or  is  associated  with,  some  valvular 
lesion  or  arterial  change,  or  some  cause  of  capillary  obstruc- 
tion, all  of  which  modify,  or  to  a  greater  or  less  extent  ob- 
scure, the  phenomena  which  attend  the  hypertrophy. 

Total  eccentric  hypertrophy  usually  cannot  be  detected 
except  by  a  physical  exploration  of  the  chest.  There  are, 
however,  certain  objective  symptoms  which  are  important, 
and  which  will  aid  in  its  diagnosis.  The  direct  effect  of 
general  hypertrophy  of  the  heart  is  to  cause  an  abnormal 
fulness  of  the  arteries  and  a  lack  of  blood  in  the  veins. 
The  pulse  is  full  and  strong  ;  the  face  is  easily  flushed ; 
the  eyes  somewhat  prominent  and  brilliant,  and  there  is 
carotid  pulsation.  The  respiration  is  not  usually  disturbed 
until  the  heart  becomes  so  increased  in  size  as  to  give  rise 
to  pressure  upon  the  adjacent  lung-tissue  and  upon  the 
diaphragm ;  then  the  patient  will  have  a  sense  of  fulness 
.about  the  chest,  and  with  that  sense  of  fulness  there  will 
be  more  or  less  uneasiness  in  the  epigastrium,  and  the 
stomach  digestion  may  be  more  or  less  interfered  with.  If 
dyspnoea  is  present,  it  is  due  to  the  pressure  of  the  en- 
larged heart  rather  than  to  any  change  in  the  lung-tissue. 
This  class  of  patients,  when  excited,  are  very  apt  to  complain 
of  cardiac  palpitation.  In  almost  all  cases  there  is  some 
cerebral  hypersemia  ;  consequently  you  will  find  in  persons 
who  are  the  subjects  of  eccentric  cardiac  hypertrophy,  that 
alcoholic  stimulants,  nervous  excitement,  and  active  physical 
exercise,  cause  headache,  vertigo,  ringing  in  the  ears,  and 
bright  spots  or  flashes  before  the  eyes. 

In  such  persons  cerebral  apoplexy  may  at  any  time  occur. 


382  PHYSICAL   SIGN'S. 

In  fact,  the  majority  of  the  cerebral  apoplexies  which  oc- 
cur in  young  subjects  are  associated  with  total  or  slight 
cardiac  hypertrophy.  It  is  now  well  established  that  there 
is  close  connection  between  atheroma  of  the  arteries  and  car- 
diac hypertrophy.  Some  observers  claim  that  the  cardiac 
hypertrophy  is  secondary  to  the  arterial  changes  ;  but  it  is 
a  fact  of  every-day  observation  that  hypertrophy  from  val- 
vular changes  will  give  rise  to  atheromatous  changes  in  the 
arteries,  for  reasons  which  have  already  been  fully  consid- 
ered in  connection  with  the  history  of  valvular  diseases. 
The  steps  of  the  change  are,  first,  cardiac  hypertrophy ; 
second,  endocarditis  ;  and  lastly,  atheroma. 

Thus,  it  will  be  seen  that  although  the  general  symptoms 
of  this  affection  are  not  readily  recognized,  yet,  when  con- 
sidered in  connection  with  its  physical  signs,  the  diagnosis 
is  generally  very  easily  made. 

PHYSICAL  SIGISTS. — The  physical  signs  of  cardiac  hypertro- 
phy will  vary  with  the  seat  and  extent  of  the  hypertrophy. 

When  it  is  general,  upon  inspection  you  will  notice  that 
although  the  heart' s  action  is  regular,  there  is  an  increased 
area  of  visible  impulse  ;  there  is  a  visible  motion  with  each 
cardiac  pulsation  over  and  even  beyond  the  entire  precor- 
dial  space.  In  children  there  is  often  a  visible  prominence 
of  the  precordial  space. 

On  palpation,  the  area  greatly  exceeds  that  within  which 
the  normal  apex-beat  is  felt,  and  the  impulse  has  a  heaving, 
lifting  character.  Usually,  the  apex-beat  of  a  healthy  heart 
is  perceptible  only  over  a  space  corresponding  to  one  or  two 
intercostal  spaces  ;  while  the  shock  of  a  hypertrophied  heart 
may  be  perceptible  over  the  whole  precordial  space  ;  and  in 
cases  of  extensive  hypertrophy,  the  head  of  the  listener  is 
often  lifted  by  the  shock.  When  the  right  ventricle  is  the 
seat  of  the  hypertrophy,  the  thoracic  wall  between  the  apex 
and  the  lower  edge  of  the  sternum,  or  even  the  sternum  it- 
self, is  shaken,  causing  a  strong  epigastric  impulse.  When 
the  left  ventricle  is  the  seat  of  the  hypertrophy,  the  apex- 
beat  is  felt  farther  to  the  left  than  natural,  sometimes  three 
inches  below,  and  three  or  four  inches  to  the  left  of  the  nor- 
mal position. 


CAEDIAC  HYPEETEOPHY. 

In  total  eccentric  hypertrophy,  the  cardiac  impulse  is  dif- 
ferent, both  longitudinally  and  transversely. 

The  apex-beat  in  hypertrophy  of  the  right  ventricle  will 
be  carried  to  the  left  and  upward  ;  whereas,  in  hypertrophy 
of  the  left  ventricle,  the  apex-beat  will  be  carried  to  the  left 
and  downward. 

On  percussion,  when  general  cardiac  hypertrophy  is  pres- 
ent, the  normal  area  of  cardiac  percussion  dulness,  both 
deep-seated  and  superficial,  will  be  increased  to  the  right  or 
left  or  downward.  The  dulness  does  not  increase  upward, 
except  in  rare  instances,  when  the  auricles  are  not  only  hy- 
pertrophied  but  dilated. 

If  the  hypertrophy  is  confined  to  the  right  ventricle,  the 
area  of  dulness  may  extend  considerably  to  the  right  of  the 
sternum  ;  while  if  the  hypertrophy  is  confined  to  the  left 
side  of  the  heart,  the  area  of  dulness  may  extend  considera- 
bly beyond  the  left  nipple.  It  is  by  these  signs  that  you 
decide  whether  right  or  left  side  hypertrophy  exists. 

The  area  of  superficial  cardiac  dulness  will  correspond  to 
that  portion  of  the  heart  which  is  uncovered  by  lung- 
tissue.  When  eccentric  hypertrophy  of  the  left  ventricle 
is  present,  the  superficial  area  of  dulness  will  be  increased 
to  the  left ;  when  the  same  condition  of  hypertrophy  is 
present  in  the  right  ventricle,  the  superficial  area  of  dulness 
will  be  increased  to  the  right. 

Usually,  it  is  not  necessary  to  resort  to  percussion  in 
order  to  determine  if  cardiac  hypertrophy  is  present.  By 
palpation  you  readily  determine  the  position  and  charac- 
ter of  the  apex-beat ;  if  you  find  it  far  to  the  left  of  its  nor- 
mal position,  and  of  a  heaving,  lifting  character,  you  may 
be  certain  that  there  is  hypertrophy  of  the  left  ventricle. 

On  auscultation,  you  will  notice  that  the  first  sound  of 
the  heart,  if  not  accompanied  by  a  murmur,  is  dull,  muf- 
fled, and  prolonged,  in  some  cases  greatly  increased  in  in- 
tensity. If  the  hypertrophy  is  confined  to  the  left  ventricle, 
the  second  sound  heard  over  the  aortic  orifice  is  increased 
in  intensity  ;  if  the  right  ventricle  is  hypertrophied,  the 
second  sound  over  the  pulmonic  orifice  will  be  increased 
in  intensity.  I  have  noticed  in  extensive  hypertrophy,  that 


384  DIFFEEENTIAL   DIAGNOSIS. 

often  both  sounds  of  the  heart  have  a  kind  of  metallic  ring, 
which  is  unnatural.  You  will  also  find  that  there  is  a 
diminution  or  an  entire  absence  of  the  respiratory  murmur 
over  the  normal  precordial  region. 

In  this  connection,  it  is  necessary  to  call  your  attention 
to  the  fact,  that  not  unfrequently  you  will  find,  when  ex- 
tensive pulmonary  emphysema  exists,  although  the  heart 
may  be  very  much  increased  in  size,  the  increase  in  the 
volume  of  the  lungs  so  shut  over  the  heart,  that  notwith- 
standing its  hypertrophied  condition,  the  apex-beat  will  not 
be  very  much  increased  in  force,  and  the  heart-sounds  will 
be  diminished  rather  than  increased  in  intensity. 

It  may,  however,  be  assumed  that  when  extensive  pul- 
monary emphysema  is  present,  and  is  attended  by  venous 
pulsation  in  the  neck,  there  is  hypertrophy  and  dilata- 
tion of  the  right  ventricle,  and  perhaps  you  may  be  able 
by  careful  percussion  to  determine  the  existence  of  an  ab- 
normal area  of  cardiac  dulness  on  the  right  side. 

DIFFERENTIAL  DIAGNOSIS. — The  diagnosis  of  cardiac  hy- 
pertrophy is  not  usually  very  difficult. 

The  distinctive  characteristic  signs  of  eccentric  hyper- 
trophy of  the  left  ventricle,  the  most  common  form  of  car- 
diac enlargement,  are  as  follows  :  a  full,  strong  pulse,  carotid 
pulsation, — flushed  countenance, — prominent  and  brilliant 
eyes,  an  abnormally  forcible  apex-beat,  which  is  visible 
over  an  unnatural  area,  more  marked  below  and  to  the  left 
of  the  normal  position  of  the  apex-beat, — an  increased  area 
of  cardiac  dulness,  also  to  the  left  and  downward, — increase 
in  the  intensity  of  the  heart-sound,  especially  of  the  second 
sound  over  the  aortic  orifice. 

The  distinctive  points  in  the  diagnosis  of  eccentric  hyper- 
trophy of  the  right  ventricle,  the  next  in  order  of  frequency, 
are  a  forcible  heart's  action  noticeable  along  the  sternum 
and  the  left  lobe  of  the  liver,  the  apex-beat  being  carried  to 
the  left  and  upward  rather  than  downward,  the  cardiac  im- 
pulse reaches  nearer  to  the  median  line  than  normal,  giving 
rise  to  a  more  or  less  marked  epigastric  impulse  ;  an  in- 
creased area  of  cardiac  dulness  to  the  right,  increased 
intensity  of  the  pulmonic  sounds,  and  more  than  normal 


CARDIAC   HYPERTROPHY.  385 

intensity  of  the  first  sound  of  the  heart  near  the  median 
line.  The  two  latter  are  the  most  reliable  signs  in  the 
diagnosis  of  hypertrophy  of  the  right  ventricle. 

The  diagnostic  signs  of  total  eccentric  cardiac  hypertro- 
phy are  similar  to  those  of  eccentric  hypertrophy  of  the 
left  ventricle,  except  that  the  area  of  cardiac  dulness  is 
increased  in  all  directions,  and  all  the  heart-sounds  are 
more  intense  than  normal. 

In  the  differential  diagnosis  of  enlargements  of  the  heart, 
you  are  liable  to  confound  cardiac  hypertrophy,  first,  with 
cardiac  dilatations  ;  second,  with  thoracic  aneurism  ;  third, 
with  mediastinal  tumors ;  fourth,  with  consolidation  of 
lung-tissue  which  may  surround  the  heart.  Under  certain 
circumstances,  pleuritic  effusion  may  be  confounded  with 
cardiac  hypertrophy.  Its  differential  diagnosis  can  better 
be  considered  in  connection  with  cardiac  dilatation.  I  will 
therefore  defer  its  further  consideration  until  we  have  com- 
pleted the  study  of  the  latter  affection. 

PROGNOSIS. — Cardiac  hypertrophy  admits  of  a  more 
favorable  prognosis  than  any  other  cardiac  affection.  In 
almost  all  instances  it  is  compensatory  by  its  development, 
the  urgent  symptoms  of  some  other  cardiac  affection  are 
relieved,  and  life  is  prolonged. 

Simple  cardiac  hypertrophy,  unless  the  result  of  aortic 
stenosis,  may  exist  for  years  without  the  occurrence  of  any 
dangerous  or  very  troublesome  symptoms. 

Slight  hypertrophy  of  the  left  ventricle  is  very  common 
in  those  who  have  led  an  active  life,  and  have  been  com- 
pelled to  perform  active  and  prolonged  physical  labor  ;  the 
hypertrophy  is  no  more  than  is  required  to  maintain  an 
equilibrium  in  the  circulation,  and  in  no  way  interferes 
with  duration  of  life.  The  patient  should  not  be  made 
aware  of  the  presence  of  such  hypertrophy,  for  although 
there  is  no  danger  attending  it,  a  knowledge  of  the  fact  may 
greatly  alarm  him.  When,  however,  cardiac  hypertrophy 
is  present,  in  which  there  is  not  only  hypertrophy,  but 
degeneration  of  the  hypertrophied  walls,  the  result  of  im- 
perfect nutrition,  after  the  manner  already  described,  the 

prognosis  is  very  unfavorable. 
25 


386  TEEATME^T. 

The  prognosis  in  hypertrophy  of  the  right  ventricle  is  by 
no  means  as  favorable  as  in  hypertrophy  of  the  left  side  of 
the  heart ;  because  it  must  inevitably  be  accompanied  by 
considerable  pulmonary  obstruction,  and  consequently  is 
rapidly  progressive. 

It  is  hardly  necessary  for  me  to  say  that  the  prognosis  in 
any  case  of  cardiac  hypertrophy  depends  upon  the  cause  of 
the  hypertrophy.  The  reason  for  this  is  apparent. 

"We  now  come  to  the  subject  of  treatment. 

TREATMENT. — Although  we  cannot  expect  by  any  mode 
of  treatment  to  cure  cardiac  hypertrophy,  still  much  can 
be  done  to  arrest  its  development  by  removing  the  causes 
which  produce  it,  or  by  rendering  them  inoperative. 

Patients  with  cardiac  hypertrophy  must  avoid  alcoholic 
stimulants.  They  also  should  avoid  immoderate  eating, 
active  and  prolonged  physical  exercise,  and  mental  excite- 
ment ;  these  are  things  especially  to  be  avoided. 

All  those  conditions  which  interfere  with  the  general  cir- 
culation, if  possible,  must  be  removed.  This  embraces  in- 
terference with  the  abdominal  circulation,  as  well  as  the 
pulmonary  and  systemic. 

Straining  at  stool  and  constipation  should  be  avoided  by 
daily  keeping  the  bowels  freely  moved.  This  condition  of 
the  bowels  should  be  maintained  chiefly  by  habits  of  life 
and  regulation  of  diet,  cathartics  being  resorted  to  only  in 
exceptional  cases 

Any  symptoms  of  cerebral  oppression  must  be  immedi- 
ately relieved  by  those  means  which  diminish  the  force  of 
the  heart' s  action.  When  the  pulse  is  full  and  strong,  and 
there  are  evidences  of  cerebral  hyperaemia,  it  has  been  the 
practice  of  some  to  bleed  the  patient,  but  this  treatment  is 
contra-indicated,  for  the  presence  of  angemia  greatly  aggra- 
vates the  dangers  arising  from  cardiac  hypertrophy.  The 
symptoms  must  be  very  urgent  to  warrant  resorting  to  it.  Of 
all  the  remedial  agents  which  diminish  the  force  of  the  heart' s 
action,  I  have  found  aconite  the  best.  When  given  in  full 
doses,  it  is  more  reliable  than  any  other  means  I  have  em- 
ployed. You  may  administer  every  three  or  four  hours 
from  two  to  three  drops  of  Fleming' s  tincture  of  the  root. 


CAEDIAC   HYPERTEOPIIY.  387 

No  drug  that  I  have  used  so  fully  and  promptly  relieves 
the  vertigo  and  other  painful  sensations  that  attend  cardiac 
hypertrophy.  Whenever  the  dilatation  of  the  cavities  ex- 
ceeds the  hypertrophy  of  the  cardiac  walls,  aconite  does 
harm. 

The  use  of  digitalis  is  contra-indicated,  unless  there  is 
degeneration  of  the  hypertrophied  cardiac  walls  ;  for,  its 
action  is  to  increase  rather  than  to  diminish  the  force  of  the 
heart's  action. 

Unquestionably  it  is  one  of  our  most  reliable  agents  in 
those  diseases  of  the  heart  in  which  the  heart' s  action  is 
enfeebled,  but  it  should  never  be  given  in  those  cases  where 
the  force  of  the  heart' s  action  is  increased. 

I  shall  tell  you  hereafter  to  administer  digitalis  in  chronic 
Bright' s  disease,  although  hypertrophy  of  the  left  ventricle 
is  one  of  its  most  constant  attendants,  but  I  advise  its  ad- 
ministration for  the  relief  of  the  kidneys,  which,  when  re- 
lieved, give  secondary  relief  to  the  hypertrophied  heart. 
Besides,  in  many  cases  of  Bright' s  disease,  the  heart,  al- 
though hypertrophied,  is  not  able  to  overcome  the  obstruc- 
tion to  the  circulation  in  the  small  arteries  and  capillary 
vessels,  and  the  tonic  effect  of  the  digitalis  raises  the  heart- 
power  to  the  point  where  the  obstruction  is  overcome  and 
the  equilibrium  of  the  circulation  established. 


LECTURE    XXXIII. 


CAKDIAC  DILATATION. 

Definition. — Varieties. 

I  WILL  now  invite  your  attention  to  the  subject  of  cardiac 
dilatation,  which  in  its  causation  and  anatomical  changes 
is  closely  allied  to  cardiac  hypertrophy. 

By  the  term  cardiac  dilatation  you  may  understand  a 
condition  of  the  heart  in  which  there  is  an  increase  in  the 
capacity  of  its  cavities ;  but  the  contractile  power  of  the 
organ  is  diminished. 

There  are  three  recognized  forms  or  stages  of  cardiac  dila- 
tation. 

First : — SIMPLE  CARDIAC  DILATATION,  in  which  the  capa- 
city of  the  heart-cavities  is  increased  without  any  marked 
change  in  the  cardiac  walls.  Such  a  condition  is  apt  to  occur 
in  connection  with  convalescence  from  any  disease  in  which 
there  has  been  great  impairment  of  nutrition,  such  as  typhoid 
fever,  etc. 

Second: — HYPERTROPHOUS  CARDIAC  DILATATION. — In  this 
form  there  is  increase  in  the  heart-cavities,  accompanied  by  a 
slight  increase  in  the  thickness  of  the  heart-walls  ;  but  the 
contractile  power  of  the  heart  is  diminished.  This  condition 
may  occur  as  the  result  of  a  degeneration  of  eccentric  hyper- 
trophy, or  it  may  occur  independent  of  any  hypertrophy 
of  the  cardiac  walls. 

TJiird: — ATROPHIC  CARDIAC  DILATATION. — In  this  form 
the  capacity  of  the  heart  cavities  is  markedly  increased,  and 
the  cardiac  walls  are  thinner  than  normal.  Sometimes  the 
ventricular  walls  diminish  to  not  more  than  two  or  three  lines 
in  thickness,  and  the  auricular  walls  may  become  so  thinned 
that  they  will  present  the  appearance  of  a  simple  membrane. 


CAEDIAC   DILATATION.  889 

Under  these  circumstances  the  contractile  power  of  the  heart 
is  almost  lost. 

^  Anatomically  as  well  as  clinically  the  significance  of  car- 
diac dilatation  is  in  proportion  to  the  excess  of  the  capacity 
of  the  cavities  over  the  thickness  of  the  cardiac  walls.  A 
cardiac  cavity  may  be  very  much  increased  in  capacity,  but 
so  long  as  there  is  a  corresponding  increase  in  the  muscular 
power  of  its  walls  sufficient  to  meet  the  demand  for  the  in- 
creased work  they  are  called  upon  to  perform,  there  will  be 
little  or  no  disturbance  to  the  general  circulation.  Eccentric 
hypertrophy  and  hypertrophous  dilatation  approach  each 
other  very  closely,  and  it  is  often  very  difficult  to  draw  the 
line  of  separation  between  them. 

MORBID  ANATOMY.— One  or  all  of  the  heart-cavities  may 
be  the  seat  of  dilatation.  The  shape  of  a  heart  when  it  has  un- 
dergone dilatation  is  changed  according  to  the  cavity  which 
is  the  seat  of  the  dilatation.  If  the  dilatation  is  confined  to 
the  right  ventricle,  the  heart  will  be  increased  in  breadth ; 
while  if  the  dilatation  affects  mainly,  or  only,  the  left  ven- 
tricle, the  heart  will  be  increased  in  length.  Ordinarily  when 
one  cavity  is  dilated,  the  remaining  cavities  are  more  or  less 
affected  in  the  same  manner. 

Cardiac  dilatation  occurs  most  frequently  in  the  auricles  ; 
next  in  the  right  ventricle,  and  last  of  all  in  the  left  ventricle. 
While  the  left  ventricle  is  less  liable  than  the  right  to  be- 
come the  seat  of  dilatation,  it  is  more  liable  to  become  the 
seat  of  hypertrophy.  When  all  the  cavities  are  dilated,  the 
entire  organ  is  increased  in  size,  and  assumes  rather  an 
ovoid  shape. 

When  the  ventricles  are  excessively  dilated,  the  trabecu- 
Ise  are  sometimes  reduced  to  the  condition  of  fleshy  tendi- 
nous cords.  When  the  walls  of  the  left  ventricle  are  very 
much  thinned,  they  collapse  when  the  ventricle  is  cut. 

The  anatomical  changes  which  take  place  in  the  muscular 
tissue  of  the  dilated  cardiac  walls,  vary  with  the  degenera- 
tive process  which  precedes  and  attends  the  dilatation. 
When  it  results  from  pericarditis  or  myocarditis,  there  is 
serous  infiltration  and  granular  degeneration  of  the  muscu- 
lar fibres  ;  when  it  is  the  result  of  fatty  metamorphosis,  the  - 


390  ETIOLOGY. 

muscular  fibres  undergo  fatty  degeneration,  the  process  of 
which  will  be  described  under  the  head  of  fatty  heart. 

In  hypertrophous  dilatation  it  is  often  impossible,  even  by 
a  microscopic  examination,  to  determine  the  exact  changes 
which  the  muscular  fibres  undergo  ;  the  abnormal  state  of 
the  muscular  fibres  can  only  be  determined  by  the  other 
evidences  of  feeble  heart-power. 

You  must  be  careful  not  to  mistake  a  heart  distended 
with  blood  and  relaxed  by  putrefaction,  for  a  dilated  heart. 

The  distinctive  marks  of  a  heart  softened  by  the  putrefac- 
tion processes  are  its  extreme  softness,  its  saturation  with 
the  coloring  matter  of  the  blood,  and  the  evidences  of  de- 
composition in  other  parts  of  the  body. 

Closely  connected  with  the  morbid  anatomy  of  cardiac 
dilatation,  is  its  causation. 

ETIOLOGY. — The  causes  of  cardiac  dilatation  vary.  One 
class  of  causes  may  be  included  under  the  head  of  the  imme- 
diate changes  which  take  place  in  the  muscular  tissue  of  the 
walls  of  a  heart  that  has  undergone  dilatation.  I  have  al- 
ready referred  to  these.  First :  we  have  the  changes  in  the 
muscular  tissue  which  accompany  pericarditis  and  en- 
docarditis. Second:  fatty  degeneration  of  the  muscular 
fibres.  Third  :  a  cardiac  dilatation  which  occurs  with  certain 
forms  of  protracted  disease,  such  as  typhoid  fever,  when 
the  most  careful  microscopical  examination  will  fail  to  de- 
tect any  uniform  change  in  the  muscular  fibre,  except  per- 
haps a  general  atrophy  of  all  the  tissues.  One  or  all  of 
these  tissue  changes  may  be  regarded  as  causes  of  cardiac 
dilatation. 

Again,  all  the  causes  of  cardiac  hypertrophy  may  become 
the  causes  of  dilatation  in  a  heart  which  has  a  feeble  resist- 
ant power.  This  group  of  causes  may  be  classed  under 
three  heads. 

First :  internal  pressure  during  a  cardiac  diastole. 
The  wall  of  a  heart  may  become  weakened  by  the  changes 
which  occur  in  certain  prolonged  diseases,  or  it  may  become 
the  seat  of  serous  infiltration  or  fatty  degeneration ;  then, 
an  abnormal  pressure  within  its  cavities  during  its  diastole 
will  cause  the  cardiac  walls  to  yield  beyond  their  normal 


CAEDIAC   DILATATION.  391 

limits.  Such  distention  is  certain  to  be  followed  by  perma- 
nent dilatation  of  its  cavities.  Most  of  the  valvular  lesions 
which  have  recently  occupied  our  attention  may  be  the  di- 
rect cause  of  such  internal  pressure  during  the  cardiac  dias- 
tole, after  the  manner  I  have  already  described  in  connection 
with  the  etiology  of  cardiac  hypertrophy. 

Generally  (as  I  have  endeavored  to  show  you),  when  the 
cardiac  cavities  become  distended  beyond  their  normal  lim- 
its, and  thus  temporarily  lose  their  contractile  power,  rapid 
hypertrophy  of  the  cardiac  walls  is  developed,  which  com- 
pensates and  to  a  certain  extent  overcomes  the  dilatation. 
But,  if  the  cardiac  walls  are  enfeebled  by  any  of  the  degen- 
erative changes  to  which  I  have  referred,  such  compensatory 
hypertrophy  does  not  take  place.  Any  valvular  lesion 
which  will  permit  a  double  current  of  blood  to  flow  into  a 
cardiac  cavity  during  its  diastole,  the  heart-walls  having 
become  enfeebled  by  degenerative  changes,  will  give  rise  to 
dilatation. 

Second :  when  the  muscular  tissue  of  a  heart  is  the  seat 
of  primary  fatty  degeneration,  after  a  time  dilatation  of  the 
cavities  takes  place,  the  normal  blood-pressure  being  suffi- 
cient to  produce  the  dilatation  ;  in  the  same  manner  will  a 
heart  become  dilated  when  its  walls  are  the  seat  of  myocar- 
ditis. 

That  form  of  cardiac  dilatation  which  follows  typhus  and 
typhoid  fever,  or  chlorosis,  usually  disappears  when  the 
attenuated  muscular  fibres  of  the  heart,  with  the  general 
muscular  system,  regain  their  normal  condition ;  but  the 
dilatation  which  results  from  fatty  degeneration  of  the 
muscular  walls  of  the  heart  steadily  increases. 

Third :  there  is  still  another  cause  of  cardiac  dilatation 
which  has  already  been  referred  to  in  connection  with  the 
history  of  valvular  diseases,  that  is,  degeneration  of  the 
muscular  substance  of  the  heart,  which  is  the  seat  of  ec- 
centric hypertrophy  ;  the  manner  of  its  development  I  have 
already  described. 

The  dilatation  does  not  occur  in  this  class  of  cases  until 
long  after  the  development  of  the  valvular  diseases  which 
give  rise  to  hypertrophy.  Usually,  the  hypertrophy  be- 


392  SYMPTOMS. 

comes  very  extensive  before  the  degenerative  dilatation 
commences,  but  when  it  once  begins  it  progresses  very 
rapidly,  and  the  failure  of  the  heart-power  is  attended  by 
very  distressing  symptoms.  The  power  which  obstruction 
to  the  pulmonary  circulation  has  to  produce  dilatation  of 
the  right  ventricle,  has  been  considered  in  connection  with 
valvular  diseases  of  the  heart.  When  these  obstructions 
exist,  eccentric  hypertrophy,  rather  than  dilatation,  is  gen- 
erally developed. 

SYMPTOMS. — The  symptoms  that  attend  the  development  of 
cardiac  dilatation  chiefly  depend  upon  the  character  and  seat 
of  the  dilatation.  In  simple  cardiac  dilatation,  the  heart- 
walls  are  of  normal  power,  but  the  capacity  of  the  cavities 
is  increased,  and  the  amount  of  blood  to  be  expelled  with 
each  cardiac  pulsation  is  greater  than  normal ;  consequently 
there  is  labored  action  of  the  heart  (often  to  such  an  extent 
that  it  may  readily  be  mistaken  for  the  action  of  a  hyper- 
trophied  heart),  yet  the  force  of  the  heart' s  action  does  not 
increase,  and  therefore  we  have  a  feebleness  of  the  radial 
pulse.  The  rhythm  of  the  heart's  action  will  not  be  dis- 
turbed. 

In  that  form  termed  atrophic  dilatation,  you  have  a  very 
different  state  of  aifairs.  The  heart- cavities  are  not  only 
dilated,  but  the  walls  of  the  cavities  are  thinner  than 
normal ;  the  heart-power  is  insufficient  for  the  expulsion 
of  the  blood  from  its  cavities,  and  as  a  result  there  is  a 
labored  action,  a  markedly  feeble  radial  pulse,  and  the 
heart,  on  account  of  the  increased  amount  of  labor,  staggers 
in  its  action,  the  arteries  are  imperfectly  filled  with  blood, 
the  veins  become  over-distended,  the  rhythm  of  the  heart's 
action  is  disturbed,  and  the  radial  pulse  becomes  weak  and 
intermitting.  These  latter  are  points  of  special  importance 
as  aifecting  the  question  of  prognosis,  for  if  a  patient  has 
all  the  symptoms  of  cardiac  dilatation  without  an  irregular 
and  intermitting  pulse,  the  prognosis  is  comparatively 
good. 

The  same  disturbance  of  the  circulation  occurs  in  that 
form  of  dilatation  which  is  developed  from  the  degeneration 
of  eccentric  hypertrophy. 


CAKDIAC   DILATATION.  393 

The  first  and  perhaps  the  most  constant  symptom  which 
is  common  to  all  varieties  of  cardiac  dilatation,  is  cardiac 
palpitation.  At  times  this  palpitation  is  very  severe  and 
distressing.  There  is  almost  constantly  a  sense  of  painful 
pulsation  in  the  region  of  the  heart.  Very  soon  after  the 
palpitation  has  manifested  itself,  the  patient  will  begin  to 
suffer  from  dyspnoaa  on  slight  exertion  ;  when  he  is  per- 
fectly quiet  he  suffers  very  little.  As  the  irregularity  of 
the  heart's  action  and  the  palpitation  increases,  the 
patient's  countenance  assumes  a  pale,  languid,  anxious 
expression,  with  more  or  less  lividity  of  the  lips.  On  excite- 
ment, or  active  physical  exertion,  the  entire  face  and  neck 
become  livid  ;  the  pulse,  which  usually  is  regular,  for  a 
time  becomes  irregular  and  intermittent.  In  this  condition, 
patients  often  live  some  time  in  comparative  comfort, — but 
they  are  conscious,  not  only  of  a  loss  of  physical,  but  of 
mental  power,  and  they  are  troubled  with  dyspeptic  symp- 
toms and  a  sense  of  fulness  about  the  epigastrium.  As 
the  disease  advances,  and  the  cardiac  dilatation  reaches  a 
point  at  which  it  is  always  troublesome,  the  patient  has 
constant  dyspnoea,  which  becomes  severe  on  slight  exer- 
tion, the  cardiac  palpitation  is  always  present,  and  often 
accompanied  by  attacks  of  syncope.  The  countenance 
assumes  a  still  more  anxious  expression,  and  the  lips  retain 
a  constant  lividity  ;  the  pulse  is  still  more  irregular  and 
intermitting.  With  these  symptoms  there  will  be  scanti- 
ness of  urine,  which  will  be  very  likely  to  contain  albumen  ; 
the  feet  and  ankles  become  oedematous,  the  oedema  gradu- 
ally extending  upward  until  the  patient  is  in  a  state 
of  general  anasarca.  The  respiration  now  becomes  very 
difficult,  so  much  so  that  the  patient  cannot  lie  down,  but 
is  obliged  to  sit,  with  his  head  inclined  forward  and  resting 
on  some  firm  support ;  he  is  unable  to  utter  more  than  a 
single  word  at  a  time.  The  extremities  become  cold  and 
blue  ;  the  mind  wanders,  and  the  patient  dies  from  general 
anasarca  with  pulmonary  O3dema. 

In  nearly  all  cases  of  cardiac  dilatation,  when  the  dila- 
tation is  extensive,  the  surface  will  have  a  yellow  tinge, 
showing  that  the  circulation  through  the  liver  is  more 


394  PHYSICAL   SIGNS. 

or  less  disturbed.  During  the  latter  stage  of  this  affection, 
most  violent  paroxysms  of  dyspnoea  will  occur,  in  some  of 
which,  it  seems  as  though  the  patient  must  die — yet  they 
rarely  prove  fatal,  but  the  patient  passes  into  a  state  of 
coma  and  dies  unconscious. 

In  extensive  cardiac  dilatation  there  is  always  danger 
from  sudden  syncope,  which  may  prove  immediately  fatal. 

To  describe  to  you  the  phenomena  that  attend  all  the 
different  degrees  of  cardiac  dilatation,  modified  as  they  are 
by  the  idiosyncrasies  of  the  individual,  as  well  as  by  the 
varying  extent  of  the  valvular  changes  which  may  be  pres- 
ent, would  be  almost  an  endless  task.  The  phenomena 
already  described  which  are  present  to  a  certain  extent  in  all 
cases,  are  sufficient  to  lead  to  at  least  a  problematical  diag- 
nosis. 

Besides,  the  physical  signs  of  this  affection,  if  properly 
appreciated,  are  very  distinctive,  and  generally  will  remove 
all  doubts  in  connection  with  a  case.  You  must  be  pre- 
pared, however,  to  find  that  the  symptoms  which  develop 
in  different  cases  greatly  vary,  but  the  variation  depends 
more  upon  the  valvular  lesions  which  are  developed  in  the 
course  of  the  dilatation  than  upon  the  dilatation  itself. 

PHYSICAL  SIGNS. — Upon  inspection,  it  will  be  noticed  that 
the  visible  area  of  the  cardiac  impulse  is  increased  ;  but  it 
is  so  indistinct  that  it  will  be  difficult  to  determine  by  in- 
spection the  exact  point  where  the  apex  of  the  heart  strikes 
the  walls  of  the  chest.  This  is  especially  the  case  if  the  chest- 
walls  are  covered  with  adipose  tissue,  or  are  at  all  oedematous. 

In  persons  with  thin  chest-walls,  you  will  sometimes 
notice  an  undulating  motion  over  the  whole  of  the  pre- 
cordial  space  ;  the  precordial  region  is  never  prominent,  as 
is  sometimes  seen  in  eccentric  hypertrophy. 

Upon  palpation,  you  will  readily  distinguish  dilatation 
from  hypertrophy  by  the  feebleness  of  the  cardiac  impulse. 
Although  it  can  sometimes  be  felt  as  far  to  the  left  as  the 
axillary  line,  yet  there  is  an  absence  of  the  lifting,  forcible 
impulse  which  attends  cardiac  hypertrophy.  It  is  often 
difficult  to  determine  the  exact  pomt  of  its  maximum  inten- 
sity, but  it  will  be  noticed  that  over  the  entire  precordial 


CAKDIAC  DILATATION.  395 

apace  there  is  an  undulating  motion,  and  the  apex-beat  will 
be  diffused,  wanting  in  power,  and  resembling  a  feeble  step. 

Sometimes  with  this  character  of  apex  beat,  a  purring 
thrill  may  be  obtained.  I  stated  to  you  that  a  purring 
thrill  with  the  apex-beat  was  almost  characteristic  of  mitral 
stenosis  ;  you  may,  however,  have  a  purring  thrill  with 
mitral  regurgitation,  when  the  regurgitation  is  associated 
with  cardiac  dilatation. 

Percussion  shows  a  greatly  increased  area  of  lateral  dul- 
ness.  The  area  will  be  increased  to  the  right,  if  the  right 
side  of  the  heart  is  the  seat  of  the  dilatation  ;  in  some  cases, 
the  increase  will  extend  an  inch  or  more  to  the  right  of  the 
sternum.  If  the  left  side  of  the  heart  is  the  seat  of  the  dila- 
tation, the  area  of  dulness  will  be  increased  to  the  left,  and 
it  may  extend  well  into  the  axillary  space. 

The  shape  of  the  increased  precordial  area  will  be  oval. 
This  point  is  of  importance  in  the  differential  diagnosis  be- 
tween cardiac  dilatation  and  pericardial  effusion. 

The  area  of  the  superficial  cardiac  dulness  is  not  increased 
in  the  same  proportion  as  the  deep-seated,  as  is  the  case  in 
cardiac  hypertrophy. 

Dilated  auricles  are  recognized  by  an  upward  increase  in 
the  area  of  dulness. 

When  the  jugular  veins  are  permanently  dilated  and 
knotted,  the  existence  of  dilatation  of  the  right  auricle  will 
not  be  difficult  to  determine. 

Auscultation.— -The  sounds  of  a  dilated  heart  are  short, 
abrupt,  and  feeble  ;  the  second  sound  is  often  inaudible  at 
the  apex,  and  the  two  sounds  are  of  very  nearly  equal 
duration.  Whenever  a  cardiac  murmur  has  existed  prior 
to  the  development  of  the  dilatation,  as  the  dilatation  de- 
velops, the  rhythm  of  the  murmur  is  lost,  and  it  becomes 
simply  a  confused  murmuring  sound. 

This  condition  has  been  denominated  asystolism.  It  is  a 
condition  in  which  you  are  unable  to  determine  whether 
the  murmur  is  synchronous  with  the  first  or  second  heart- 
sound  ;  pauses  or  intermissions  occur  at  irregular  intervals, 
which  are  of  more  frequent  occurrence  during  exercise  than 
when  the  patient  is  quiet.  When  the  asystolic  condition  is 


396  DIFFERENTIAL   DIAGNOSIS. 

present,  the  prognosis  is  very  unfavorable,  independent  ol 
the  general  condition  of  the  patient,  for  it  shows  that  in 
addition  to  the  valvular  lesions  which  may  be  present, 
cardiac  dilatation  has  been  developed  to  such  an  extent  as 
to  give  rise  to  complete  confusion  of  the  normal  heart- 
sounds  ;  under  such  conditions,  the  patient  is  liable  to  die 
at  any  moment. 

Asystolism  is  generally  accompanied  by  a  diffused  cardiac 
impulse,  which  is  peculiar,  and  readily  appreciated  by  the 
ear,  as  it  rests  over  the  precordial  space. 

The  respiratory  murmur  is  diminished  in  intensity  over 
the  whole  of  the  upper  portion  of  the  left  lung. 

DIFFERENTIAL  DIAGNOSIS. — The  diagnosis  of  dilatation 
of  the  heart  rests  mainly  on  the  following  conditions  :  Fee- 
ble action,  undulating  impulse,  indistinctness  of  apex-beat ; 
lateral  increase  in  the  area  of  percussion  dulness,  very 
nearly  square  in  its  outline  ;  short,  abrupt,  and  feeble  heart- 
sounds  ;  a  feeble,  irregular,  and  intermitting  pulse,  accom- 
panied by  the  general  symptoms  of  systemic  and  pulmo- 
nary obstruction  and  congestion. 

The  differential  diagnosis  between  cardiac  hypertrophy 
and  cardiac  dilatation  is  never  very  difficult.  The  symp- 
toms of  the  two  conditions  differ  very  materially.  For  in- 
stance, the  heart- sounds  are  intensified  in  hypertrophy 
and  feeble  in  dilatation.  In  both  cases  we  have  an  in- 
creased area  of  apex-beat,  yet  in  hypertrophy  it  is  full,  dis- 
tinct, and  forcible,  while  in  dilatation  it  is  feeble,  diffused, 
and  indistinct. 

An  individual  with  cardiac  hypertrophy  apparently  has 
a  more  than  normally  vigorous  and  forcible  action  of  the 
heart,  which  is  increased  by  active  exercise ;  he  has  none 
of  the  feebleness  which  attends  the  person  with  cardiac 
dilatation.  The  fact  that  an  individual  has  had  cardiac 
hypertrophy  with  all  its  attendant  symptoms,  but  now  has 
a  tired  expression  of  countenance,  livid  lips,  his  physical 
vigor  daily  growing  less  and  less,  accompanied,  it  may  be, 
by  oedema  of  the  feet,  shows  that  cardiac  hypertrophy  has 
become  cardiac  dilatation. 

Dilatation  of  the  right  side  of  the  heart,  in  addition  to 


CAKDIAC   DILATATION".  397 

the  signs  already  detailed,  is  to  be  recognized  by  changes 
produced  in  the  veins.  The  presence  of  distended,  irregular, 
turgid,  jugular  veins  tells  very  positively  of  dilatation  of 
the  right  auricle  ;  and  pulsation  in  the  jugulars,  with  feeble 
heart-action  and  increase  in  the  area  of  cardiac  dulness 
upon  the  right,  very  plainly  shows  dilatation  of  the  right 
ventricle  associated  with  tricuspid  regurgitation. 

It  is  sometimes  somewhat  difficult  to  make  a  differential 
diagnosis  between  pericarditis  with  effusion  and  cardiac 
dilatation.  In  pericarditis  with  effusion,  the  area  of  dul- 
ness is  increased,  and  there  is  a  feeble  apex-beat,  and  some- 
times an  undulating  impulse,  all  of  which  are  present  in 
cardiac  dilatation.  The  heart-sounds  in  pericarditis  are 
more  removed  from  the  surface  than  they  are  in  dilatation, 
and  the  area  of  percussion  dulness  is  pyriform  in  shape, 
while  in  dilatation  it  assumes  a  square  shape.  Besides 
these  distinguishing  features,  you  will  rarely  meet  with  a 
case  of  pericarditis,  even  with  effusion,  when  you  may  not 
hear  a  friction- sound  at  some  point ;  but  in  cardiac  dilata- 
tion there  is  an  entire  absence  of  friction-sound. 

In  addition  to  these  differences  in  the  physical  signs,  the 
history  of  the  case  and  the  accompanying  rational  symp- 
toms will  be  of  great  assistance  in  solving  the  question  of 
differential  diagnosis  between  either  cardiac  dilatation  and 
pericarditis,  or  cardiac  hypertrophy  and  fluid  in  the  peri- 
cardial  sac.  The  differential  diagnosis  between  enlargement 
of  the  heart,  either  from  dilatation  of  its  cavities  or  hyper- 
trophy of  its  walls,  and  thoracic  tumors,  will  sometimes 
present  itself.  Both  of  these  cardiac  conditions  may  be 
developed  as  the  result  of,  or  in  connection  with,  thoracic 
aneurisms.  One  very  reliable  differential  sign  is  the  direc- 
tion of  the  increased  area  of  percussion  dulness  in  thoracic 
aneurisms  and  mediastinal  tumors ;  they  always  enlarge 
upward  and  to  the  right  or  left,  while  in  cardiac  enlarge- 
ment the  area  of  dulness  is  increased  latterly  and  down- 
ward. This  fact,  taken  in  connection  with  the  other  physi- 
cal and  rational  signs  of  aneurism,  is  generally  sufficient  for 
the  differential  diagnosis  between  these  conditions. 

Consolidation  of  lung-tissue  in  the  region  of  the  heart 


398  PROGNOSIS. 

may  give  rise  to  some  of  the  signs  of  cardiac  enlargement, 
but  the  other  attending  physical  signs  of  pulmonary  con- 
solidation will  enable  you  to  distinguish  between  the  dul- 
ness  on  percussion  produced  by  the  pulmonary  consolida- 
tion and  the  increased  area  of  dulness  produced  by  cardiac 
enlargements. 

PROGNOSIS. — The  prognosis  in  cardiac  dilatation  is  always 
bad,  and  the  danger  to  life  is  increased  in  proportion  to  the 
excess  of  the  capacity  of  the  cavities  over  the  thickness  of 
their  walls.  The  greater  the  increase  in  the  capacity  of  the 
cavities,  and  the  greater  the  diminution  in  the  thickness  of 
the  cardiac  walls,  the  greater  will  be  the  danger  to  life. 
Feebleness  of  the  general  muscular  system,  and  impoverish- 
ment of  the  blood  greatly  increases  the  danger.  If  patients 
have  been  subject  to  paroxysms  of  dyspnoea  and  attacks  of 
syncope,  the  prognosis  is  especially  bad,  for  then  there  is 
constant  danger  of  sudden  death. 

The  dangers  attending  any  intercurrent  pulmonary  dis- 
ease are  always  great. 

Whenever  dropsy  of  any  kind  has  been  developed,  the 
prognosis  is  very  bad  ;  under  such  conditions  few  patients, 
even  with  the  best  of  care,  live  more  than  eighteen  months  ; 
the  majority  die  within  a  year.  In  those  cases  in  which  the 
pulse  is  regular,  or  only  becomes  irregular  after  violent 
physical  exertion,  the  prognosis  is  comparatively  good ; 
much  can  be  done  to  relieve  and  prolong  the  life  of  such 
patients.  When  general  anasarca  has  been  developed,  and 
the  patient  is  no  longer  able  to  assume  the  recumbent  pos- 
ture, you  may  be  able  to  give  temporary  relief,  but  it  will  be 
only  temporary.  This  brings  us  to  the  question  of  treatment. 

TREATMENT. — As  regards  complete  recovery,  the  treat- 
ment of  cardiac  dilatation  is  altogether  unsuccessful.  It  is 
not  a  curable  disease.  Even  the  good  effects  of  palliative 
measures  are  only  temporary.  There  are,  however,  two  im- 
portant results  to  be  accomplished  in  the  management  of  a 
case  of  cardiac  dilatation. 

First,  the  nutrition  of  the  body  must  be  maintained  at 
its  highest  point  as  the  most  certain  means  of  preventing 
flaccidity  of  the  cardiac  walls. 


CAKDIAC   DILATATION.  399 

Second,  all  irregular  or  violent  action  of  the  heart,  as 
far  as  possible,  must  be  prevented. 

To  accomplish  the  first  result,  the  diet  must  be  most 
nutritious,  taken  in  small  quantities,  and  at  short  intervals. 
An  exclusive  milk  diet  will  often  be  found  most  advantage- 
ous to  this  class  of  patients  ;  stimulants  must  be  taken 
only  in  small  quantities  and  with  the  food.  When  symp- 
toms of  anaemia  are  present,  iron  may  also  be  administered 
with  the  food  ;  as  a  rule,  it  is  always  safe  to  daily  adminis- 
ter iron  to  a  patient  with  dilated  heart. 

The  greatest  amount  of  fresh  air,  and  the  best  hygienic 
influences  should  be  secured.  The  skin  should  be  kept 
active,  slightly  stimulating  baths  may  be  employed  for  the 
purpose  of  increasing  the  power  of  the  capillary  circulation. 

To  accomplish  the  second  result,  this  class  of  patients 
must  be  placed  under  the  strictest  rules  in  regard  to  exer- 
cise. They  should  never  allow  themselves  to  be  placed  in 
such  circumstances  as  to  render  necessary  sudden  and  vio- 
lent exercise  ;  for  a  single  violent  physical  exertion  may 
jeopardize  the  life  of  any  patient  with  cardiac  dilatation. 

Every  exertion  of  this  character  carries  the  point  of  resist- 
ance in  the  cardiac  wall  a  little  beyond  what  it  can  ever 
regain.  Flannel  should  be  worn  next  the  skin.  A  dry,  brac- 
ing air  generally  best  agrees  with  this  class  of  patients.  As 
regards  the  medicinal  agents  to  be  employed  in  the  manage- 
ment of  cardiac  dilatation,  each  case  must  be  studied  by  itself. 

All  discharges  that  are  exhausting  must  be  arrested.  If 
hypersemia  of  the  liver  and  other  abdominal  viscera  exist, 
it  must  be  relieved  by  the  occasional  administration  of  an 
aloetic  or  mercurial  purge ;  excessive  purgation  is  not 
admissible,  but  a  daily  movement  of  the  bowels  without 
exhausting  cathartics  is  important.  When  there  is  loss  of 
appetite  and  impaired  digestion,  vegetable  tonics  and  min- 
eral acids  are  indicated. 

Those  remedial  agents  which  have  a  direct  effect  upon  the 
heart  itself  are  all  important  in  the  management  of  this  form 
of  cardiac  disease.  The  most  important  and  most  servicea- 
ble of  this  class  of  remedies  is  digitalis.  It  can  always  be  ad- 
ministered in  full  doses,  or  at  least  in  sufficiently  large  doses 


400  TKEATMEXT. 

to  regulate  the  heart's  action.  Often  when  the  feet  become 
cedematous  and  the  patient  cyanotic,  it  has  a  wonderful 
effect,  entirely  removing,  at  least  for  a  time,  all  unpleasant 
symptoms.  When  the  heart' s  action  becomes  regular,  the 
digitalis  may  be  given  in  smaller  doses,  but  the  small  doses 
must  be  continued  for  a  long  time. 

If,  after  a  time,  the  heart' s  action  cannot  be  controlled  by 
the  digitalis,  belladona  or  opium  may  be  combined  with  it ; 
the  effect  of  the  combination  is  to  tranquillize  the  excited 
heart,  which  tranquillizing  effect  is  only  temporary,  and  they 
should  only  be  resorted  to  when  the  digitalis  has  been 
thoroughly  tested  and  has  failed. 

In  the  use  of  digitalis  the  same  restriction  is  to  be  ob- 
served which  was  spoken  of  in  connection  with  the  treatment 
of  other  cardiac  diseases,  that  is,  that  it  should  never  be  used 
indiscriminately,  for  the  time  will  come  when  the  remedy 
will  cease  to  have  its  controlling  effect,  and  then  we  are  help- 
less. It  is  always  desirable  to  postpone  that  period  as  long 
as  possible. 

Should  the  heart  become  nervously  excited  during  the 
administration  of  the  digitalis,  as  it  often  does,  the  various 
antispasmodic  remedies  may  be  employed. 

Paroxysms  of  dyspnoea  may  be  temporarily  relieved  by 
hydrocyanic  acid,  cannabis  Indica,  ether,  and  dry  cupping 
along  the  spine.  During  the  slow  progress  of  a  chronic  case 
of  cardiac  dilatation,  a  great  variety  of  measures  may  be  in- 
dicated and  afford  temporary  relief  ;  still,  our  chief  reliance 
will  always  be  upon  digitalis  and  iron,  combined  with  the 
most  nutritious  diet  and  absolute  rest. 


LECTURE  XXXIV. 


•CARDIAC  DEGENERATIONS. 

Myocarditis. — Fatty  Degeneration  of  the  Heart. 

THIS  morning  I  shall  commence  the  history  of  the  degen- 
erations of  the  cardiac  walls. 

The  first  to  which  your  attention  is  directed  is  myocarditis. 
I  class  this  among  the  cardiac  degenerations,  for  all  its  pro- 
cesses are  degenerative. 

By  the  term  myocarditis  is  understood  an  inflammation 
of  the  muscular  structure  of  the  heart,  attended  by  degen- 
eration and  softening  of  the  primitive  muscular  fibre. 

This  disease  may  be  general  or  local.  General  diffused 
myocarditis  is  undoubtedly  a  rare  affection.  Circumscribed 
or  local  myocarditis  is  of  quite  frequent  occurrence,  espe- 
cially that  form  which  only  involves  the  external  or  internal 
surface  of  the  heart,  and  is  met  with  in  connection  with  peri- 
carditis and  endocarditis. 

MORBID  ANATOMY. — The  diseased  process  consists  in 
changes  which  take  place  either  in  the  primitive  bundles  of 
muscular  fibre,  or  in  the  intermuscular  areolar  tissue. 

These  changes  have  all  the  characteristics  of  inflamma- 
tion. When  the  change  primarily  affects  the  primitive 
fibrillse  of  the  muscle,  it  is  termed  parenchymatous  myocar- 
ditis. When  the  change  primarily  affects  the  areolar  tissue, 
it  is  called  interstitial  myocarditis.  Although  these  two 
varieties  may  not  be  recognized  during  life,  they  are  very 
readily  recognized  after  death.  Any  portion  of  the  muscu- 
lar tissue  of  the  heart  may  be  the  seat  of  the  inflammatory 

27 


402  MORBID   ANATOMY. 

process ;  the  portion  most  frequently  affected  is  the  left 
ventricle. 

The  first  change  that  can  be  noticed  in  that  portion  of  the 
heart  which  is  the  seat  of  the  myocarditis,  is  a  change  in 
color  ;  at  first,  the  muscle  assumes  a  dark  red  color, — later, 
it  assumes  a  grayish,  and  finally  it  changes  to  a  dark 
green  color.  If,  therefore,  at  the  post-mortem  examina- 
tion, you  find  any  portion  of  the  muscular  tissue  of  the 
heart  of  a  dark  green  color,  unless  the  change  has  been 
produced  by  post-mortem  changes,  you  may  safely  assume 
that  the  patient  had  myocarditis. 

The  microscopical  appearances  of  a  portion  of  the  mus- 
cular tissue  which  is  the  seat  of  myocarditis,  will  vary  with 
the- stage  of  the  inflammation.  At  first,  it  may  be  noticed, 
that  the  primitive  bundles  are  large  and  have  a  swollen  ap- 
pearance, which  is  due  to  an  infiltration  of  serum  ;  their 
striae  become  indistinct.  Later,  the  fibrillse  break  down 
into  a  finely  granular  detritus,  and  more  or  less  extensive 
fatty  metamorphosis  occurs. 

Still  later,  you  find  the  muscular  fibre  replaced  by  con- 
nective tissue ;  or  the  generative  process  may  go  on  until 
you  have  breaking-down  of  tissue,  accompanied  by  forma 
tion  of  abscesses. 

In  other  words,  myocarditis  terminates  either  in  connec- 
tive-tissue formation  or  in  abscess.  You  may  readily  ap- 
preciate how  essentially  these  terminations  differ. 

When  a  large  extent  of  the  muscular  tissue  of  the  ven- 
tricular wall  is  occupied  by  new  connective- tissue  forma- 
tion, the  power  of  resistance  of  the  ventricular  wall  is 
diminished,  so  that,  during  the  ventricular  diastole  the  new 
connective  tissue  is  liable  to  become  gradually  and  slowly 
stretched,  and  finally  it  gives  rise  to  what  is  called  aneurism 
of  the  heart. 

This  is  the  manner  in  which  aneurisms  of  the  heart  are 
most  commonly  formed. 

Calcareous  matter  may  also  be  deposited  in  the  newly 
formed  connective  tissue,  and  then  we  have  a  cardiac  aneu- 
rism with  calcareous  deposits  in  its  walls. 

When  the  inflammatory  process  takes  a  more  degenera- 


MYOCARDITIS.  403 

tive  course  and  terminates  in  the  formation  of  an  abscess, 
the  molecular  degeneration  replaces  more  and  more  the  mus- 
cular fibres,  until  finally  you  find  a  collection  of  purulent 
fluid  in  the  midst  of  softened  and  degenerated  muscular 
substance  ;  this  form  is  not  met  with  except  in  pyaemia  and 
low  forms  of  fever. 

As  a  result  of  this  gradual  destruction  of  muscular  tissue, 
rupture  of  the  heart  may  take  place,  and  then  you  will 
find  at  the  post-mortem  examination  the  pericardium  more 
or  less  distended  with  blood,  and  if  an  opening  is  found  in 
the  cardiac  wall,  you  may  safely  assume  that  the  rupture 
has  occurred  in  consequence  of  the  degenerative  changes 
which  have  been  developed  in  connection  with  myocarditis. 

How  myocarditis  differs  from  the  muscular  softening  that 
occurs  when  high  temperature  is  maintained  for  a  long 
time,  is  not  yet  determined  ;  it  seems  to  differ  only  in 
degree. 

ETIOLOGY. — The  causes  of  myocarditis,  endocarditis,  and 
pericarditis  are  almost  identical.  Rheumatism,  the  most 
frequent  cause  of  pericardial  and  endocardia!  inflammation, 
becomes  a  frequent  cause  of  myocarditis.  It  is  maintained 
by  some  that  endocarditis  and  pericarditis  never  occur  with- 
out producing  some  degree  of  myocarditis ;  but  in  most 
cases,  under  such  circumstances,  the  myocarditis  is  so 
slight  that  it  hardly  affects  our  diagnosis  or  prognosis. 

In  rare  instances  myocarditis  is  the  result  of  embolism  of 
the  coronary  arteries  ;  such  cases  are  exceedingly  rare,  but 
the  specimen  which  I  now  present  to  you  is  a  well-marked 
example  of  this  class. 

Again,  myocarditis  occurs  in  connection  with  all  septic 
diseases,  such  as  pyaemia,  septicsemia,  typhus,  and  typhoid 
fevers. 

The  myocarditis  which  occurs  with  pyaemia  generally 
terminates  with  the  formation  of  abscesses ;  that  which  occurs 
with  rheumatism  usually  terminates  in  connective-tissue 
formations.  Indeed,  in  a  large  proportion  of  rheumatic 
hearts  you  will  find  at  the  apex  of  the  left  ventricle  an 
increase  of  connective  tissue,  showing  that  there  has  been  a 
previous  myocarditis.  The  increase  which  is  seen  is  some- 


404  SYMPTOMS. 

thing  more  than  the  simple  increase  of  endocardial  tissue  in 
connection  with  the  process  of  endocarditis  ;  it  is  the  result 
of  a  myocarditis  which  has  terminated  in  connective- tissue 
formations. 

Occasionally  this  affection  has  its  starting-point  in  syphi- 
litic connective-tissue  changes. 

I  have  never  met  with  traumatic  myocarditis,  and  suppose 
it  to  be  rare.  High  temperature  long  continued,  perhaps, 
may  be  a  cause  of  myocarditis. 

SYMPTOMS. — There  are  no  distinctive  symptoms  of  myo- 
carditis. In  a  large  majority  of  instances,  during  life,  it  is 
impossible  to  positively  determine  its  existence.  It  is  main- 
tained by  some  that  a  mild  form  complicates  every  case  of 
pericarditis  and  endocarditis ;  but  its  existence  under  such 
circumstances  is  a  matter  of  inference  rather  than  of  posi- 
tive diagnosis.  A  rapid,  feeble,  compressible,  and  un- 
certain pulse  coming  on  suddenly  in  the  course  of  an  acute 
endocarditis  or  pericarditis,  is  the  most  reliable  of  all 
symptoms. 

Pain  in  the  precordial  region,  accompanied  by  an  irregular 
and  disturbed  action  of  the  heart  during  the  course  of  an 
acute  inflammatory  affection  of  the  heart,  furnishes  good 
reason  for  suspecting  that  myocarditis  is  present.  Then 
the  principal  symptoms  which  should  lead  you  to  suspect 
its  existence,  are  attacks  of  cardiac  palpitation,  a  feeble, 
irregular,  intermitting  pulse,  attacks  of  syncope  on  active 
physical  exertion,  and  all  the  phenomena  which  attend  a 
failure  of  heart-power ;  if  these  come  on  suddenly  in  one 
who  is  known  to  be  the  subject  of  acute  endocarditis  or 
pericarditis,  or  who  is  suffering  from  some  severe  septic 
form  of  disease,  you  have  reason  to  suspect  myocarditis. 
There  are  no  physical  signs  except  those  common  to  all  con- 
ditions of  heart  failure.  If,  however,  the  myocarditis  has 
terminated  in  connective-tissue  formations,  and  aneurism  of 
the  ventricular  wall  has  occurred  as  the  result,  you  may  be 
able  to  recognize  its  occurrence  by  a  change  in  the  shape  of 
the  heart.  The  area  of  precordial  dulness  will  be  increased 
upward  and  toward  the  left  shoulder  rather  more  than  when 
there  is  cardiac  hypertrophy  or  dilatation.  There  will  be 


MYOCAEDITIS.  405 

the  absence  of  the  heaving  impulse  of  cardiac  hypertrophy, 
and  it  will  be  that  of  cardiac  dilatation.  The  diagnosis  of 
myocarditis  can  only  be  conjectural.  It  is  probable  that  it 
has  much  to  do  with  most  of  the  sudden  deaths  which 
occur  in  the  progress  of  pericarditis  or  endocarditis. 

When  abscess  of  the  heart  occurs  as  a  termination  of  this 
aifection,  it  will  probably  go  unrecognized  until  the  post- 
mortem examination,  as  during  life  there  are  no  means  of 
ascertaining  the  existence  of  this  condition. 

There  are  no  points  in  connection  with  its  differential 
diagnosis  that  are  of  any  practical  value,  as  there  are  no 
constant  or  distinctive  signs  of  its  existence. 

PROGNOSIS. — General  myocarditis,  if  it  ever  occurs,  must 
of  necessity  prove  fatal ;  circumscribed  myocarditis  may  be 
recovered  from.  The  present  state  of  our  clinical  knowledge 
of  the  disease  admits  only  of  a  speculative  prognosis,  based 
rather  on  our  knowledge  of  its  pathological  lesions  than  on 
any  symptoms  which  these  changes  may  give  rise  to.  Ex- 
tensive connective-tissue  formations  frequently  found  in  the 
cardiac  walls  give  evidence  that  circumscribed  myocarditis 
is  frequently  recovered  from  ;  but  the  extent  and  stage  at 
which  recovery  is  possible,  and  what  symptoms  indicate  a 
certainly  fatal  termination,  is  still  undetermined.  At  times, 
it  is  undoubtedly  the  precursor  of  fatty  degeneration  of  the 
heart. 

TREATMENT. — If  you  have  reason  to  suspect  the  existence 
of  myocarditis  in  the  course  of  an  endocarditis  or  pericar- 
ditis, you  will  not  materially  change  your  plan  of  treatment ; 
it  is  essentially  the  same  as  that  already  indicated  for  the 
management  of  those  affections.  There  is  one  thing  of 
great  importance  to  be  remembered,  and  that  is,  great  care 
should  be  exercised  not  to  overtax  the  heart.  All  active 
and  prolonged  physical  exertion  must  be  prohibited.  This 
class  of  patients  should  never  be  allowed  to  give  any  in- 
creased labor  to  the  heart,  until  some  time  has  elapsed  after 
convalescence  has  been  established.  It  is  important  always 
to  carry  nutrition  to  its  highest  point,  to  guard  against  the 
development  of  fatty  degeneration.  It  is  quite  probable 
that  many  cases  of  fatty  heart  are  the  sequelae  of  myocar- 


406  MORBID   ANATOMY. 

ditis.  Not  unfrequently,  septic  and  fever  patients,  after 
violent  physical  exertion  during  convalescence,  suddenly 
die ;  death,  under  such  circumstances,  is  sometimes  the  re- 
sult of  over-taxation  of  a  heart  weakened  by  myocarditis. 
Besides  absolute  rest,  and  the  sustaining  measures  already 
referred  to,  about  all  that  can  be  done  with  these  patients 
is  to  treat  symptoms  as  they  develop. 

FATTY  DEGENERATION  OF  THE  HEART. 

This  is  probably  the  most  common  form  of  cardiac  degen- 
eration. It  may  involve  the  entire  organ,  or  it  may  be 
confined  to  one  portion.  When  it  is  circumscribed,  it  has 
a  local  cause. 

There  are  two  morbid  processes  connected  with  fatty 
degeneration  of  the  heart.  First,  fatty  degeneration  of  the 
primitive  muscular  fibre,  what  is  termed  "Quain's  fatty 
degeneration"  of  the  heart ;  this  is  by  far  the  most  impor- 
tant degeneration.  Second,  the  deposit  of  fat  in  the  areolar 
tissue  of  the  heart,  or  the  connective  tissue,  is  replaced  by 
fat ;  this  form  affects  the  muscular  fibre  merely  by  pressure 
on  it. 

These  two  conditions  differ  very  materially,  both  in  the 
pathological  changes  which  have  taken  place,  and  in  the 
effects  which  they  may  produce. 

MORBID  ANATOMY. — When  fatty  degeneration  of  the 
heart  is  confined  to  the  muscular  fibre,  the  first  change 
which  will  be  noticed  is,  that  the  primitive  fibre-bundles 
lose  their  nuclei,  their  striated  appearance  disappears,  and 
they  become  granular ;  the  granules  appear  to  completely 
fill  the  sarcolemma.  This  granular  material  at  first  pre- 
sents the  appearance  of  albuminous  matter  ;  soon,  however, 
the  sarcous  substance  gives  place  to  fat  granules  and  to  oil- 
globules,  which  are  arranged  more  or  less  evenly  in  rows. 
but  eventually  they  entirely  take  the  place  of,  or  fill  the 
Barcolemma.  The  degenerated  fibres  are  of  the  same  size  as 
the  normal  fibres.  When  these  changes  have  taken  place, 
the  muscular  tissue  assumes  a  yellow  or  dirty -brown  color  ; 
it  has  lost  its  power  of  resistance,  and  breaks  down  very 


FATTY  DEGENEKATION  OF  THE  HEAKT.       407 

readily  under  pressure  ;  the  heart  in  most  instances  retains 
its  normal  size ;  it  may  be  hypertrophied ;  it  is,  however,  more 
commonly  dilated  ;  the  coronary  arteries  may  be  atheroma- 
tous,  calcified,  obliterated,  or  normal.  There  is  no  neces- 
sary relation  between  morbid  conditions  of  these  vessels 
and  this  form  of  degeneration,  although  when  the  degener- 
ation occurs  secondary  to  muscular  hypertrophy,  the  coro- 
nary circulation  is  more  or  less  interfered  with.  In  the 
other  form  of  fatty  change  of  the  heart,  you  will  discover 
simply  an  increase  of  fat  in  the  areolar  tissue  of  the  heart ; 
this  fat  does  not  interfere  with  the  formation  of  muscular 
fibre  except  by  its  pressure.  If  the  fatty  accumulation  is 
extensive,  it  may  interfere  materially  with  the  muscular 
fibres  of  the  heart,  on  account  of  the  pressure  which  it  may 
produce.  Thus  you  see  that  there  is  a  radical  difference 
between  these  two  forms  of  degeneration. 

The  first  form  of  fatty  degeneration  may  cause  death  by 
so  weakening  the  walls  of  the  heart  that  rupture  will  take 
place,  or  by  so  weakening  the  contractile  power  of  the 
heart  as  to  render  it  incapable  of  performing  its  function. 

The  second  form,  or  fatty  infiltration,  may  somewhat 
diminish  the  heart-power,  but  it  rarely  if  ever  can  be  re- 
garded as  directly  or  indirectly  a  cause  of  death. 

ETIOLOGY. — All  the  causes  of  fatty  degeneration  of  the 
muscular  fibrillse  of  the  heart,  or  true  fatty  metamorphosis, 
as  yet  are  undetermined.  It  is  evident,  however,  that  any- 
thing which  interferes  with  the  nutrition  of  the  heart,  tends 
to  fatty  degeneration  of  its  walls. 

Although  it  is  occasionally  met  with  in  young  persons,  it 
is  essentially  a  disease  of  middle  and  advanced  life.  This 
tendency  to  fatty  changes  comes  on  with  senile  decay. 

It  is  often  one  of  the  most  prominent  signs  of  that  maras- 
mus which  comes  on  in  connection  with  Bright' s  disease, 
chronic  alcoholismus,  gout,  phthisis,  cancer,  etc. ;  when  de- 
veloped in  this  connection,  it  never  reaches  a  point  where  it 
seriously  interferes  with  the  action  of  the  heart. 

In  quite  a  large  proportion  of  cases,  fatty  degeneration  of 
the  heart  is  the  result  of  mal-nutrition  from  some  interfer- 
ence with  the  supply  of  blood  through  the  coronary  arteries. 


408  SYMPTOMS. 

Such  interference  may  arise  from  atheroma  or  calcification 
of  the  coronary  vessels,  embolic  obstruction,  external  com- 
pression from  pericardial  thickenings,  or  impairment  of  the 
aortic  recoil  from  any  cause.  As  has  already  been  shown, 
a  hypertrophied  or  dilated  heart  is  very  apt  to  undergo 
fatty  change  from  this  cause.  Fatty  heart  has  been  met 
with  in  connection  with  poisoning  by  phosphorus,  phos- 
phoric acid,  etc. 

There  is  a  certain  class  of  persons  who  have  fatty  degen- 
eration of  the  heart,  and  yet  are  apparently  healthy.  This 
fatty  degeneration  seems  to  be  due  to  a  hereditary  predispo- 
sition ;  it  is  the  same  degenerative  tendency  which  mani- 
fests itself  in  other  tissues  of  the  body,  and  must  be  regarded 
as  due  to  a  certain  constitutional  tendency,  which  is  either 
hereditary  or  acquired — its  exact  nature  is  undetermined. 

Disease  of  the  cardiac  ganglia  and  nerves  may  lead  to 
fatty  heart. 

Fatty  infiltration  of  the  heart,  or  the  deposit  of  fat  in  its 
areolar  tissue,  occurs  as  a  part  of  general  obesity,  which  so 
frequently  develops  after  persons  have  passed  middle  life. 
It  is  quite  frequently  met  with  in  connection  with  chronic 
alcoholismus,  and  it  may  be  found  in  persons  who  have 
suffered  from  cancer,  phthisis,  and  other  wasting  affections. 

SYMPTOMS. — The  symptoms  which  are  indicative  of  fatty 
heart  are  never  apparent  until  the  degenerative  process  has 
become  quite  extensive.  Moderate  fatty  degeneration  of 
the  heart  will  go  unrecognized  ;  sudden  death  has  occurred 
from  this  cause  when  there  was  no  suspicion  of  its  existence. 
As  a  rule,  the  progress  of  the  disease  is  very  gradual  and 
insidious,  and  most  of  the  symptoms  which  attend  its  de- 
velopment are  due  to  feeble  action  of  the  heart. 

Persons  who  are  the  subjects  of  extensive  fatty  degenera- 
tion of  the  heart  cannot  undergo  active  physical  exertion 
any  length  of  time,  without  complete  exhaustion  ;  if  they 
attempt  any  active  exercise,  they  are  compelled  to  stop  and 
rest  every  few  moments.  They  have  little  muscular  power  ; 
their  skin  is  pale,  sallow,  and  at  times  more  or  less  livid ; 
their  digestion  is  feeble  ;  they  suffer  from  paroxysms  of  ex- 
treme dyspnoea  after  physical  exercise  ;  during  these  parox- 


FATTY  DEGENERATION  OF  THE  HEART.  409 

ysms  the  liver  enlarges;  their  respiration  is  feeble  and 
irregular  in  its  rhythm,  often  it  is  sighing  in  its  character. 
There  is  one  peculiarity  of  the  feebleness  which  attends  its 
development,  and  that  is  its  progressive  character.  This 
class  of  patients  are  usually  aware,  when  they  review  their 
history  for  a  few  months,  that  there  has  been  a  gradual  and 
steady  development  of  loss  of  muscular  power. 

The  tissues  are  flabby  ;  there  is  evidence  of  degeneration 
of  the  vessels.  The  arcus  senilis  has  been  considered  an 
important  sign  of  fatty  heart. 

Owing  to  the  inadequate  supply  of  blood  to  the  nerve 
centres,  peculiar  cerebral  symptoms  are  present,  such  as 
irritability  of  temper,  habitual  depression  of  spirits,  dis- 
turbance of  vision,  failure  of  memory,  giddiness,  vertigo. 
Sudden  cerebral  anaemia  may  occur  during  excitement  or 
active  physical  exercise,  inducing  syncope  or  epileptiform 
attacks.  Frequent  attacks  of  fainting  occurring  in  one 
who  has  the  symptoms  of  fatty  heart  are  always  alarming  ; 
although  in  the  majority  of  cases  they  are  readily  recovered 
from,  and  do  not  leave  any  permanent  ill  effect ;  sometimes 
these  attacks  last  for  hours. 

The  pulse  of  persons  with  fatty  heart  is  peculiar ;  it  is 
always  feeble,  and  although  it  apparently  varies  in  force, 
there  is  no  real  increase.  It  may  be  perfectly  regular  in 
rhythm,  while  the  patient  is  quiet,  yet  on  slight  exertion  it 
becomes  greatly  accelerated  and  irregular  both  in  force  and 
rhythm. 

It  may  be  very  rapid  for  some  minutes,  then  suddenly  it 
becomes  irregular,  not  beating  more  than  thirty  or  forty 
times  in  a  minute  ;  this  is  a  very  characteristic  sign  of  fatty 
heart. 

In  an  advanced  stage  of  the  disease,  in  addition  to  the 
cerebral  symptoms  already  referred  to,  patients  sometimes 
get  into  a  condition  which  bears  a  striking  resemblance  to 
that  produced  by  the  administration  of  chloroform. 

Attacks  of  angina  pectoris  sometimes  occur  in  connection 
with  the  fatty  heart.  At  one  time,  it  was  thought  that 
fatty  heart  was  the  principal  cause  of  angina  pectoris  ;  but 
now  we  regard  angina  pectoris  as  a  neurosis  depending  foi 


410  PHYSICAL   SIGNS. 

its  cause  on  a  variety  of  cardiac  lesions,  and  possibly  at 
times  occurring  independent  of  any  heart  disease.  It  is, 
therefore,  evident  that  nearly  all  the  subjective  symptoms 
which  attend  the  development  of  fatty  degeneration  of  the 
heart  are  equivocal. 

Fatty  infiltration  of  the  heart  gives  rise  to  no  functional 
disturbance  of  the  organ,  and  is  not  attended  by  any  un- 
pleasant or  dangerous  phenomena.  Should  atrophy  of  the 
muscular  substance  of  the  heart  from  pressure  of  the  fatty 
accumulation  occur  (which  seldom  happens),  the  attend- 
ing symptoms  and  results  differ  in  no  respect  from  those 
already  detailed  as  attendants  of  fatty  metamorphosis  of  the 
muscular  fibres. 

PHYSICAL  SIGNS. — The  physical  signs  of  fatty  heart  are 
negative  rather  than  positive. 

On  inspection,  the  apex-beat  will  be  indistinct,  or  if  the 
case  is  far  advanced  it  will  be  invisible. 

On  palpation,  the  hand  either  will  not  detect  any  move- 
ment over  the  precordial  space,  or  there  will  be  scarcely 
perceptible  motion  directly  over  the  apex.  If  the  fatty 
metamorphosis  has  occurred  in  a  hyper trophied  heart,  there 
will  be  a  tumbling,  rolling  motion,  similar  to  that  which 
accompanies  cardiac  dilatation,  and  it  is  really  a  sign  of 
dilatation  rather  than  of  fatty  degeneration. 

On  percussion,  the  area  of  precordial  dulness,  both  super- 
ficial and  deep-seated,  is  normal. 

Upon  auscultation,  the  first  sound  of  the  heart  will  be 
feeble  or  absent.  This  absence  of  the  first  sound  is  the 
characteristic  physical  sign  of  fatty  degeneration  of  the 
heart.  If  the  first  sound  is  heard,  it  is  short,  and  followed 
by  a  first  long  silence  ;  the  second  sound  is  also  feeble  but 
distinct. 

There  are  other  conditions  in  which  the  first  sound  of  the 
heart  is  temporarily  absent.  If  it  occurs  in  connection 
with  typhoid  fever,  or  in  the  anaemia  of  old  age,  it  will 
return  with  the  symptoms  of  convalescence  from  the  fever, 
or  with  the  disappearance  of  the  anaemia.  In  any  case, 
when  the  first  sound  of  the  heart  is  feeble  or  absent,  you 
may  not  be  able  at  your  first  or  at  a  single  examination  to 


FATTY  DEGENERATION   OF   THE  HEART.  411 

decide  that  it  is  due  to  fatty  heart ;  if,  however,  you  find 
it  continues  to  be  feeble  or  absent,  in  connection  with  the 
other  symptoms  to  which  I  have  referred  as  indicating  this 
change  in  the  heart,  you  are  warranted  in  making  the 
diagnosis  of  fatty  degeneration  of  the  heart. 

DIFFERENTIAL  DIAGNOSIS. — The  diagnosis  of  fatty  heart 
is  always  problematical,  until  the  fatty  change  is  far 
advanced.  It  may  even  then  be  confounded  with  other 
degenerations  of  the  heart,  as  amyloid  degenerations,  etc. 

The  differential  diagnosis  between  cardiac  dilatation  and 
fatty  heart  is  of  the  most  importance,  and  at  times  the 
most  difficult  to  make.  In  dilatation,  you  will  have  feeble- 
ness, irregular  pulse,  vertigo,  ringing  in  the  ears,  and 
attacks  of  syncope ;  all  of  these  symptoms  present  in  the 
one  case  are  also  present  in  the  other,  but  from  the  general 
symptoms  of  the  patient  and  the  physical  signs  present, 
you  will  usually  be  able  to  draw  the  line  of  distinction. 
A  dilated  heart  occupies  an  abnormal  space  in  the  thoracic 
cavity,  and  will  consequently  give  rise  to  an  abnormal  area 
of  cardiac  dulness  ;  while  the  area  of  a  fatty  heart  does  not 
exceed  the  normal  area.  There  will  usually  be  little  doubt 
of  the  existence  of  a  fatty  heart  in  an  individual  who  has 
a  feeble  heart-action,  indistinct  first  sound,  with  a  distinct 
second  sound,  attended  by  no  cardiac  murmur.  We  may 
be  still  more  certain  of  its  existence,  if  the  precordial  dul- 
ness is  of  normal  area,  the  pulse  feeble  and  irregular,  the 
respiration  ascending  and  descending  in  rhythm,  and  if,  be- 
sides, we  have  the  peculiar  cerebral  manifestations  de- 
scribed as  present  in  persons  with  fatty  heart. 

If  fatty  degeneration  accompanies  cardiac  dilatation,  there 
will  be  a  greater  disturbance  of  the  heart' s  action  than  is 
present  in  fatty  degeneration  without  dilatation. 

PROGNOSIS.— The  prognosis  in  fatty  degeneration  of  the 
muscular  fibrillse  is  bad  ;  the  tendency  of  the  degeneration 
is  steadily  to  advance,  for  it  is  a  decay  which  nothing  can 
prevent.  It  is  true  that  persons  with  fatty  heart  may  live 
for  years,  but  when  the  disease  reaches  an  a-dvanced  stage 
life  is  very  insecure.  The  fatal  termination  may  occur 
quite  suddenly  from  syncope,  from  rupture  of  the  heart,  or 


412  TREATMENT. 

as  the  result  of  cerebral  anaemia ;  it  may  also  terminate 
slowly  by  asthenia,  which  is  usually  attended  by  general 
dropsy. 

TREATMENT. — There  is  no  plan  of  treatment  to  be  adopted 
with  any  prospect  of  restoring  the  degenerated  muscular 
fibres  of  the  heart.  The  great  and  perhaps  the  only  object 
to  be  attained  in  the  treatment  of  fatty  heart  is,  to  improve 
or  rather  increase  the  tissue-making  power  of  the  blood  ;  to 
this  end,  iron,  cod-liver  oil,  good  nutritious  diet,  with  fresh 
air  and  light  physical  exercise  may  be  employed.  If  alco- 
holic stimulants  have  been  used  habitually,  or  to  excess, 
they  must  be  stopped.  All  active  or  violent  physical 
exercise  must  be  avoided,  as  well  as  all  excitement ;  the 
life  of  the  patient  must  be  that  of  an  invalid.  By  avoid- 
ing everything  which  may  stimulate  the  heart's  action,  and 
by  the  strict  observance  of  all  the  laws  of  hygiene,  life  may 
be  prolonged.  By  these  means  you  may  succeed  in  restrain- 
ing the  progress  of  the  malady,  but  you  cannot  expect  to 
altogether  arrest  it.  Digitalis  is  of  little  or  no  use  to  this 
class  of  patients,  for  it  has  no  muscular  fibres  upon  which  to 
act ;  sometimes  its  administration  will  afford  temporary 
relief  where  there  is  yielding  of  the  cardiac  walls,  with 
venous  congestion. 

In  fatty  infiltration  of  the  areolar  tissue  of  the  heart,  the 
only  treatment  which  seems  to  be  of  any  service  is  to 
restrict  the  diet  of  the  patient,  and  place  him  under  a 
systematic  physical  training  which,  by  its  rigor,  shall 
diminish  or  remove  fatty  accumulations  in  other  parts  of 
the  body. 


LECTURE    XXXV. 


CARDIAC  DEGENERATIONS. 


Amyloid  Degeneration.  —  Muscular  Atrophy. — Rupture  of  the  Heart.— 
Aneurisms  of  the  Heart.  —  Cardiac  Thrombosis. — New  Formations  in 
the  Heart. — Neuroses  of  the  Heart. 


I  WILL  continue  the  history  of  the  degenerated  changes 
which  are  met  with  in  the  muscular  walls  of  the  heart,  by 
saying  a  few  words  concerning  amyloid  or  waxy  degenera- 
tion of  the  cardiac  walls. 

MOEBID  ANATOMY. — This  form  of  cardiac  degeneration  is 
never  met  with  except  in  connection  with  similar  changes 
in  other  organs  of  the  body,  and  is  due  to  a  constitu- 
tional cause.  It  is  of  rare  occurrence,  and  consists  in  the 
formation  of  a  shining,  colloid  material  in  the  primitive 
muscular  fibres,  which  gives  the  reaction  of  amyloid  mate- 
rial. It  is  most  frequently  found  in  the  walls  of  the  right 
ventricle,  causing  its  cut  surface  to  present  the  character- 
istic appearance  of  waxy  metamorphosis.  The  primary 
changes  take  place  in  the  sarcolemma  of  the  muscles. 

Amyloid  degeneration  of  the  cardiac  walls  is  very  often 
associated  with  the  development  of  syphilitic  gummata. 
These  masses,  when  present,  are  found  scattered  throughout 
the  substance  of  the  heart.  They  vary  in  size,  from  a  pea 
to  a  pigeon's  egg;  usually  the  largest  are  found  in  the 
septum  ventriculorum.  They  may  become  converted  into 
masses  of  connective  tissue,  or  they  may  undergo  fatty  and 
cheesy  metamorphosis. 

ETIOLOGY. — Waxy  degeneration  of  the  walls  of  the  heart, 


414  MORBID   ANATOMY. 

and  the  formation  of  gummata  in  its  substance,  are  due  to 
those  causes  which  produce  similar  forms  of  degeneration 
in  the  other  organs  and  tissues  of  the  body ;  among  these 
causes,  syphilis  stands  first. 

SYMPTOMS. — There  are  no  special  symptoms  attending 
these  degenerations,  except  those  which  are  indicative  ol 
cardiac  failure.  Their  existence  can  only  be  suspected, 
never  positively  determined. 

If  the  signs  of  cardiac  failure,  with  waxy  degeneration  oi 
other  organs,  as  the  spleen  and  liver,  are  present  in  an  indi- 
vidual who  has  never  been  the  subject  of  rheumatism  or  any 
valvular  disease,  but  who  has  a  syphilitic  diathesis,  you 
have  good  reason  to  suspect  these  degenerative  changes  in 
the  heart. 

TREATMENT. — The  treatment  is  the  same  as  in  the  advanced 
stage  of  syphilis. 

MUSCULAR  ATROPHY  OP  THE  HEART. 

Atrophy  of  the  muscular  walls  of  the  heart  may  or  may 
not  be  accompanied  by  a  change  in  the  size  of  its  cavities. 
Sometimes  its  cavities  are  dilated,  but  usually  they  are  di- 
minished in  size.  When  the  term  eccentric  atrophy  is  used, 
a  condition  of  simple  dilatation  is  indicated.  The  atrophy 
may  be  confined  to  the  walls  of  one  cavity,  or  it  may  involve 
the  walls  of  all  the  cavities  of  the  heart. 

MORBID  ANATOMY. — Some  writers  describe  atrophy  of  the 
heart  under  the  head  of  simple,  concentric  and  eccentric,  but 
these  terms  are  hardly  necessary,  as  almost  all  cases  of  car- 
diac atrophy  are  concentric,  that  is,  atrophy  of  the  cardiac 
walls  is  accompanied  by  diminution  in  the  capacity  of  its 
cavities.  In  some  cases,  wasting  of  the  cardiac  muscles  is 
attended  by  inter-muscular  connective-tissue  increase,  and 
under  these  circumstances  there  will  be  no  decrease  in  the 
size  of  the  heart,  while  there  is  a  marked  diminution  in  its 
contractile  power. 

The  atrophied  muscle  may  be  of  normal  color,  or  from  the 
presence  of  little  pigment  granules  it  may  have  a  brownish 
hue.  There  may  be  no  histological  change  in  the  muscular 


MUSCULAR  ATROPHY  OF   THE   HEART.  415 

fibres,  or  they  may  undergo  fatty  degeneration  ;  sometimes 
with  the  muscular  atrophy  there  is  an  abnormal  accumula- 
tion of  fat  beneath  the  pericardium. 

ETIOLOGY.— Any  chronic,  exhausting  disease,  as  phthisis 
pulmonalis,  cancerous  cachexia,  or  any  disease  that  is  ac- 
companied by  wasting  of  the  general  muscular  system,  may 
produce  atrophy  of  the  heart.  It  is  frequently  met  with  in 
very  aged  persons.  Atrophy  of  the  heart  also  accompanies 
extensive  chronic  pericardial  effusion,  and  is  the  result  of 
the  pressure  of  the  fluid.  Fibrous  thickening  of  the  peri- 
cardium causing  constriction  of  the  coronary  arteries,  as 
well  as  atheroma  and  thrombosis  of  the  coronary  arteries, 
may  cause  partial  or  complete  cardiac  atrophy.  Acute  in- 
fectious diseases,  when  greatly  prolonged,  may  give  rise  to 
cardiac  atrophy.  In  rare  instances  it  is  the  result  of  myo- 
carditis followed  by  fatty  or  fibrous  degeneration. 

SYMPTOMS. — Cardiac  atrophy  is  usually  attended  by  no 
special  symptoms,  as  it  is  rarely  met  with  except  in  connec- 
tion with  wasting  of  the  muscles  of  the  general  system.  It 
is  difficult  to  decide  whether  the  symptoms  indicating 
enfeebled  circulation  depend  upon  loss  of  heart -power,  or 
upon  the  general  muscular  wasting. 

The  existence  of  that  form  of  cardiac  atrophy  which  is 
met  with  in  the  aged,  cannot  be  positively  determined  dur- 
ing life. 

That  form  which  results  from  local  interference  with  the  nu- 
trition of  the  heart,  is  attended  by  symptoms  similar  to  those 
already  described  as  indicating  the  existence  of  fatty  heart. 

In  both  forms,  the  heart's  impulse  is  feeble  and  its 
sounds  indistinct. 

PROGNOSIS. — The  prognosis  depends  upon  the  cause  and 
extent  of  the  atrophy.  In  extensive  atrophy  attended  by 
fatty  degeneration,  and  in  atrophy  depending  upon  the  pres- 
sure of  a  pericardial  effusion,  the  prognosis  is  unfavorable  ; 
the  atrophy  of  old  age  is  not  attended  by  any  special  dan- 
ger to  life. 

TREATMENT. — All  that  you  can  do  in  this  disease  is  to  in 
crease  nutrition,  and  avoid  physical  exertion  and  mental 
excitement. 


416  EUPTUEE   OF   THE  HEAET. 

The  food  must  be  of  the  most  nutritions  character,  and 
wine  may  be  indulged  in  rather  freely. 

Iron,  which  is  so  serviceable  in  other  cardiac  affections 
attended  by  enfeebled  nutrition  and  failure  of  heart-power, 
will  be  found  of  some  service  in  this  condition. 


RUPTURE  OF  THE  HEART. 

Rupture  of  fhe  heart,  and  the  escape  of  blood  into  the 
pericardium,  rarely  if  ever  occurs,  unless  the  muscular 
tissue  of  the  heart  is  the  seat  of  fatty  or  some  other  form  of 
degeneration. 

The  seat  of  the  rupture  is  usually  in  the  left  ventricle, 
and  it  may  be  single  or  multiple.  The  fissure  generally 
runs  parallel  to  the  fasciculi  of  the  heart  fibres, — it  may  be 
partial  at  first,  and  complete  some  time  after  the  rupture 
commences.  It  usually  takes  place  from  within  outward, 
and  occurs  or  commences  during  the  cardiac  systole. 

ETIOLOGY. — When  rupture  of  the  heart  occurs,  it  follows 
the  various  textural  changes  in  the  heart's  substance,  to 
which  I  have  already  referred  ;  it  is  immediately  induced 
by  some  violent  physical  effort  or  mental  excitement.  If  it 
occurs  during  sleep,  or  when  the  individual  is  quiet,  there 
is  reason  to  believe  that  it  was  commenced  some  time  pre- 
vious, and  that  this  apparently  sudden  rupture  is  only 
its  completion. 

SYMPTOMS. — If  the  rupture  is  complete  and  extensive,  the 
hand  is  suddenly  carried  to  the  chest,  a  few  convulsive 
twitches  occur,  and  unconsciousness  or  death  immediately 
follows.  If  the  rupture  is  partial,  the  symptoms  are  those 
of  collapse,  and  death  may  not  occur  for  several  hours. 

Rupture  of  the  heart  sometimes  occurs  in  connection 
with  a  paroxysm  of  prsecordial  pain  resembling  angina 
pectoris. 

PROGNOSIS. — Death  is  certain,  nothing  can  avert  it. 

TREATMENT. — Necessarily,  this  can  be  only  palliative. 
Stimulants  and  narcotic?  may  be  given  to  afford  temporary 
relief. 


ANEURISM  OF  THE  HEAKT.  417 

ANEURISM  OF  THE  HEART. 

Aneurisms  of  the  heart  may  be  fusiform  or  sacculated, 
and  they  are  usually  situated  in  the  wall  of  the  left  ven- 
tricle, near  its  apex.  They  may  be  single  or  multiple. 

MOEBID  ANATOMY. — In  most  instances  cardiac  aneurisms 
form  slowly,  and  are  the  result  of  inflammatory  processes 
in  the  endocardium,  and  in  the  muscular  tissue  of  the  car- 
diac walls.  These  processes  (as  I  have  already  shown)  may 
convert  a  small  or  large  portion  of  the  muscular  wall  of  the 
ventricle  into  fibrous  tissue. 

The  portion  so  changed  yields  to  the  internal  blood  pres- 
sure, and  a  circumscribed  pouch  or  sac  is  formed,  which 
communicates  with  the  heart-cavity  by  a  small  opening.  As 
these  pouches  increase  in  size  their  walls  become  thinner, 
and  sometimes  rupture ;  they  may  undergo  calcification. 
These  sacs  may  be  partially  or  completely  filled  with  fibrin 
or  fluid  blood. 

In  rare  instances,  where  portions  of  the  cardiac  walls  have 
undergone  fatty  degeneration,  these  aneurismal  pouches 
form. 

ETIOLOGY. — Among  the  causes  of  aneurism  of  the  heart, 
may  be  included  endocardial,  pericardial,  and  myocardial 
inflammations,  as  well  as  the  different  forms  of  degenera- 
tion of  the  cardiac  walls. 

SYMPTOMS. — The  symptoms  of  this  affection  are  obscure. 
It  has  no  recorded  clinical  history  which  distinguishes  it  from 
other  diseases  of  the  ventricular  walls.  In  some  instances 
every  known  symptom  of  cardiac  disease  is  present. 

The  physical  signs  are  equally  unsatisfactory  and  unin- 
telligible. The  physical  signs  of  chronic  pericarditis,  en- 
docarditis, hypertrophy,  and  dilatation  are  sometimes  all 
present. 

PROGNOSIS. — Sudden  death  may  occur  from  rupture  of  the 
sac  into  the  pericardium,  or  the  patient  may  be  worn  out  by 
the  attendants  of  cardiac  dilatation. 

TREATMENT. — There  is  no  special  treatment  for  this  affec- 
tion. Those  means  advised  for  the  relief  of  cardiac  dilata- 
tion will  be  found  most  serviceable. 

27 


418  MORBID  ANATOMY. 

CARDIAC  THEOMBOSIS. 

At  nearly  every  autopsy  which  you  may  make,  you  will 
find  a  clot  of  blood  in  the  right  heart.  This  clot  will  be 
most  firm  in  those  who  die  of  acute  disease  ;  it  will  be  more 
or  less  adherent  to  the  cardiac  walls  and  the  trabeculse,  and 
may  extend,  like  a  cord,  into  the  vessels.  At  one  time  it 
is  entirely  composed  of  fibrin,  and  is  of  a  pale  straw-color ;  at 
another  time  it  contains  red  globules,  and  is  of  a  dark  red 
color.  These  clots  are  formed  during  the  last  hours  of  life, 
and  immediately  after  death.  They  have  no  pathological 
significance. 

MORBID  ANATOMY. — In  true  cardiac  thrombosis  coagula 
are  formed  in  the  heart-cavities  a  short  time  previous  to 
death,  or  they  may  have  existed  for  years. 

They  vary  in  size  from  a  pin' s  head  to  a  walnut,  and  may 
be  even  larger  ;  they  have  a  flattened  or  rounded  shape. 

If  they  are  of  small  size  and  firmly  adherent  to  the  valves 
or  trabeculse,  they  are  called  vegetations.  If  they  are  of 
large  size  they  are  called  thrombi,  and  may  be  found  in  any 
of  the  heart  cavities  ;  as  a  rule,  they  are  firmly  adherent  to 
the  endocardium. 

They  are  usually  met  with  in  those  hearts  which  are  the 
seat  of  valvular  diseases  that  interfere  with  the  free  circula- 
tion of  blood  through  the  heart-cavities. 

The  constitution  of  these  thrombi  varies.  Sometimes  they 
are  firm,  dry,  and  of  a  whitish  color,  composed  of  unorgan- 
ized fibrin  ;  at  other  times  they  have  a  globular  outline,  are 
firmly  attached  to  the  endocardium,  and  have  the  constitu- 
tion of  cysts,  which  contain  a  reddish  or  yellowish  green 
puriform  fluid.  These  cysts  are  formed  by  the  softening 
and  breaking  down  of  the  centres  of  solid  coagula.  They 
may  be  distinctly  fibroid  in  their  constitution,  or  pseudo- 
cartilaginous,  or  they  may  undergo  calcification. 

These  thrombi  may  remain  permanently  attached  to  the 
endocardium,  or  they  may  become  separated  from  it  in 
masses  of  considerable  size,  or  in  minute  particles.  The 
consequences  of  such  separation  are  always  serious,  giving 
rise  either  to  embolism  or  septic  infection. 


CARDIAC    THROMBOSIS.  419 

m  ETIOLOGY.— All  cardiac  thrombi  originate  in  coagula- 
tion of  the  blood.  In  some  instances,  the  coagulation  is 
rapid,  and  the  coagula  are  of  large  size  ;  in  other  instances, 
the  coagulation  is  slow,  and  the  coagula  are  of  small  size. 

The  conditions  which  favor  these  coagulations  are :  first, 
obstruction  to  the  passage  of  blood  through  the  heart ; 
second,  abnormal  changes  in  the  composition  of  the  blood  ; 
third,  endocarditis. 

Obstruction  to  the  passage  of  blood  through  the  heart 
may  be  due  to  valvular  lesions,  cardiac  dilatation,  and 
feebleness  of  the  contractile  power  of  the  heart. 

The  condition  of  the  blood  which  favors  its  coagulation 
is  that  abnormal  condition  which  we  have  in  acute  inflam- 
mation, rheumatism,  Bright' s  disease,  and  certain  acute  in- 
fectious diseases. 

Coagulation  in  endocarditis  is  due  to  the  roughening  of 
the  endocardial  surface  produced  by  the  endocardial  in- 
flammation. 

SYMPTOMS. — The  symptoms  of  cardiac  thrombosis  in  its 
gravest  form  are  urgent.  At  the  moment  of  coagulation, 
the  heart' s  action  becomes  frequent  and  irregular ;  the 
pulse  is  small,  weak,  and  irregular  in  force  and  rhythm ; 
partial  syncope,  with  restlessness  and  jactation  are  com- 
bined with  symptoms  of  more  or  less  complete  pulmonary 
obstruction.  The  brain  also  suffers  ;  this  is  indicated  by 
delirium,  convulsions,  and  finally  a  fatal  coma.  Life  is 
rarely  prolonged  beyond  the  third  day. 

In  less  grave  forms,  the  symptoms  are  not  so  urgent. 
The  dyspnoea  is  slight,  the  cyanosis  is  not  extreme,  the 
jugular  veins  are  but  slightly  distended,  the  respiration  is 
somewhat  hurried,  and  the  pulse  is  increased  in  frequency, 
and  is  intermitting.  In  a  word,  the  general  symptoms  are 
those  of  advanced  heart  disease. 

Where  the  coagula  are  of  small  size,  and  the  coagulation 
takes  place  slowly,  there  will  be  few  if  any  objective  symp- 
toms to  indicate  their  presence,  and  life  may  not  be 
seriously  endangered  ;  these  latter  cases,  however,  are  rather 
cases  of  vegetations  forming  on  the  valve  and  chordsB  ten- 
dinese,  than  true  cardiac  thrombosis. 


PHYSICAL   SIGNS. 

PHYSICAL  SIGNS. — Inspection  and  palpation  show  irreg- 
ularity in  the  cardiac  impulse.  The  area  of  cardiac  per- 
cussion dulness  is  increased  to  the  right  of  the  sternum. 

On  auscultation,  there  is  marked  irregularity  in  the 
heart-sounds.  JSTew  murmurs  are  developed ;  or  if  mur- 
murs existed  prior  to  the  occurrence  of  the  thrombosis,  they 
are  increased  in  intensity.  The  most  common  murmur  is 
that  indicative  of  obstruction  at  the  right  auriculo-ven- 
tricular  or  pulmonic  orifice,  having  its  maximum  of  in- 
tensity at  the  xiphoid  cartilage,  and  conveyed  to  the  left 
of  the  sternum.  Occasionally,  there  will  be  a  murmur  in- 
dicating obstruction  in  the  left  ventricle. 

If  the  coagula  are  of  small  size,  the  murmurs  are  similar 
to  those  which  accompany  endocarditis. 

DIFFERENTIAL  DIAGNOSIS. — The  symptoms  of  sudden 
shock  to  the  heart,  and  the  systemic  effects  of  sudden  intra- 
cardiac  obstruction,  taken  in  connection  with  the  sudden 
development  of  a  loud  cardiac  murmur,  evidently  originat- 
ing on  the  right  side  of  the  heart,  are  sufficient  to  lead  one 
to  a  problematical  if  not  a  positive  diagnosis  of  cardiac 
thrombosis. 

The  only  condition  which  is  liable  to  be  mistaken  for  it 
is  the  rupturing  of  a  valve,  or  of  one  of  the  chordae  tendi- 
nese  from  ulcerative  endocarditis.  I  know  of  no  means  by 
which  a  differential  diagnosis  can  be  made  with  any  degree 
of  certainty  until  some  time  after  the  occurrence. 

PROGNOSIS. — It  is  unfavorable  in  all  cases  of  extensive 
cardiac  thrombosis.  If  the  coagula  are  small,  it  is  possible 
for  them  to  disappear  after  a  time,  or  to  become  changed 
into  vegetations ;  but  large  cardiac  thrombi  destroy  life, 
sometimes  in  twelve  hours,  and  at  other  times  life  may  be 
prolonged  for  two  or  three  days. 

TREATMENT. — Theoretically,  carbonate  of  potassa  has  the 
power  of  arresting  or  preventing  the  formation  of  cardiac 
thrombi.  Accepting  this  theory,  some  give  sesqui-carbonate 
of  ammonia  in  endocarditis  and  pneumonia,  to  prevent  the 
formation  of  heart-clots,  which  they  believe  to  be  very  fre- 
quently the  cause  of  sudden  death  in  these  diseases.  I  am 
not  aware  that  there  is  any  positive  evidence  in  favor  of  or 


CAEDIAC    THROMBOSIS.  421 

against  this  theory.  If  there  should  be  a  tendency  to  syn- 
cope in  this  or  any  other  disease  in  which  cardiac  thrombo- 
sis is  liable  to  occur,  I  would  administer  carbonate  of  ammo- 
nia in  large  doses,  at  least  thirty  grains  every  two  hours. 

Bleeding,  and  every  agent  which  has  a  tendency  to 
enfeeble  the  heart-power,  must  be  avoided.  Absolute  quiet 
must  be  insisted  upon,  and  digitalis  and  opium  may  be 
administered  in  small  doses.  Alcoholic  stimulants  must  be 
given  with  great  care,  and  only  to  prevent  collapse. 

NEW  FORMATIONS  IN  THE  HEART. 

Morbid  growths  or  new  formations  in  the  walls  of  the 
heart  have  no  clinical  importance,  and  I  shall  only  detain 
you  with  their  enumeration. 

Cancer  of  the  heart  as  a  primary  affection  is  exceedingly 
rare  ;  while  cancerous  nodules  in  the  walls  or  on  the  surface 
of  the  heart,  in  connection  with  general  cancerous  infec- 
tion, occasionally  occur.  Under  these  circumstances,  the 
disease  usually  manifests  itself  in  the  form  of  small  circum- 
scribed medullary  or  melanotic  tumors,  which  are  devel- 
oped either  in  the  heart- walls  or  under  the  pericardium  or 
endocardium. 

When  cancer  of  the  heart  pccurs  from  the  extension  of 
cancer  of  the  neighboring  parts,  large  portions  of  the  heart 
may  become  transformed  into  cancerous  tissue.  The  exist- 
ence of  cancerous  growths  in  the  heart  cannnot  be  recog- 
nized during  life,  and  are  of  interest  only  in  connection  with 
post-mortem  examinations. 

Tubercle  is  found  in  the  heart  only  in  connection  with 
acute  tuberculosis  when  it  develops  in  the  connective  tissue. 
It  has  no  clinical  importance,  and  its  existence  cannot  be 
recognized  during  life. 

Fibroma,  lipoma,  and  myoma  are  rare  forms  of  circum- 
scribed tumors  found  in  the  cardiac  walls,  or  under  the  en- 
docardium or  pericardium.  Their  existence  cannot  be  de- 
termined during  life. 

Parasites. — The  heart  may  be  the  seat  of  parasites.  The 
echinococcus,  the  cysticercus,  and  entozoa  have  all  been 


422  MORBID  ANATOMY. 

found  in  the  heart- walls,  and  have  been  known  to  lead  to 
their  rupture,  causing  death. 

Cysts,  containing  serum  or  grumous  fluid,  have  also  been 
found  in  the  heart- walls.  All  of  these  developments  have 
the  effect  of  depressing  or  interfering  with  the  heart's  action, 
but  their  diagnosis  in  most  cases  is  impossible. 

CARDIAC  NEUROSES,  OR  NERVOUS  AFFECTIONS  OF  THE  HEART. 

There  is  great  obscurity  as  regards  nervous  affections  of 
the  heart,  both  as  to  their  etiology  and  morbid  anatomy. 

I  shall  include  under  this  head  those  forms  of  cardiac  de- 
rangement in  which  there  is  an  interference  with  the  motion 
and  sensibility  of  the  heart. 

The  two  prominent  neuroses  of  the  heart  are  nervous 
palpitation  and  angina  pectoris.  Some  regard  both  of 
these  affections  as  functional  disorders. 

NERVOUS  CARDIAC  PALPITATION. 

As  has  already  been  shown,  cardiac  palpitation  is  one  of 
the  very  common  symptoms  of  organic  disease  of  the  heart ; 
but  I  purpose  now  to  speak  of  it  only  when  it  occurs  inde- 
pendent of  organic  cardiac  disease.  Cardiac  palpitation, 
independent  of  organic  disease  of  the  heart,  is  more  common 
in  the  female  than  in  the  male.  It  comes  on  suddenly,  and 
is  generally  intermittent. 

MORBID  ANATOMY.— There  are  no  known  anatomical 
changes  either  in  the  heart  or  in  its  nerve-supply,  which 
can  be  regarded  as  the  morbid  anatomy  of  cardiac  palpita- 
tion ;  if  there  are  any  anatomical  changes,  undoubtedly 
they  have  their  seat  in  the  cardiac  plexus. 

So  long  as  our  knowledge  is  so  imperfect  regarding  the 
influence  of  the  cardiac  nerves  upon  the  functions  of  the 
heart,  we  cannot  determine  the  seat  of  the  anatomical 
changes  which  give  rise  to  the  phenomena  of  cardiac  palpi- 
tation. To  a  very  great  extent,  cardiac  palpitation  is  of 
reflex  origin. 

ETIOLOGY. — The  causes  of  this  affection  are  more  appa- 
rent, and  may  be  briefly  stated. 


CAKDIAC   PALPITATIOIST.  423 

First. — Violent  physical  exercise  or  indulgence  in  intoxi- 
cating liquors  will  accelerate  the  circulation  and  give  rise  to 
a  form  of  cardiac  palpitation  which  ceases  as  soon  as  the 
cause  is  removed. 

Second. — Adults  with  contracted  chests,  and  young  per- 
sons about  the  time. of  puberty,  whose  growth  has  been 
rapid,  often  complain  of  palpitation.  In  these  cases  it 
seems  to  be  caused  by  the  narrowness  of  the  chest,  which 
interferes  with  the  free  play  of  the  heart. 

Third. — Palpitation  is  a  very  frequent  symptom  in  states 
of  debility  or  anaemia,  from  whatever  cause  they  may  arise. 
Under  this  head  are  included  sexual  excesses,  enervating 
habits,  and  all  acute  infectious  diseases  that  are  attended 
by  extensive  nutritive  disturbances,  as  typhoid  fever,  etc. 

Fourth. — Cardiac  palpitation  is  of  frequent  occurrence  in 
persons  with  what  is  called  a  nervous  temperament,  induced 
by  late  hours,  the  habitual  use  of  strong  tea  and  coffee,  the 
inordinate  use  of  tobacco,  derangements  of  the  digestive 
organs,  sudden  shock  or  fright,  etc. 

Fifth. — Cardiac  palpitation  is  frequently  met  with  in  per- 
sons with  a  gouty  diathesis,  accompanied  by  dyspeptic 
symptoms,  which  are  attended  by  flatulence. 

SYMPTOMS. — In  a  perfectly  healthy  subject  with  a  well- 
formed  chest,  the  cardiac  impulse  is  so  slight  that  the 
motion  is  not  perceptible,  unless  the  hand  be  applied  to  the 
precordial  space.  Whenever  a  person  becomes  sensible  of  the 
beating  of  his  own  heart,  he  may  be  said  to  have  cardiac  pal- 
pitation. By  this  term  we  understand  an  unnaturally  strong 
cardiac  impulse,  attended  by  a  more  than  naturally  rapid 
action  of  the  heart,  which  may  be  irregular  and  intermitting. 

In  some  cases  of  palpitation,  the  cardiac  impulse  com- 
municates a  slight,  quick  shock  to  the  chest  walls  ;  in  other 
cases,  the  impulse  is  prolonged  and  heaving  in  character ; 
in  still  other  cases,  it  is  even  weaker  than  natural. 

The  heart- sounds  are  sometimes  increased  in  intensity  to 
such  an  extent  that  they  are  distinctly  audible  to  the 
patient  when  he  lies  on  his  left  side  ;  again,  they  are  not  in 
the  slighest  degree  increased  in  intensity.  At  one  time  the 
fits  of  palpitation  come  on  suddenly  and  are  of  short  dura- 


424  DIFFERENTIAL  DIAGNOSIS. 

tion ;  at   another  time,  they  come  on  gradually  and  are 
long  and  severe. 

Cardiac  palpitation  may  be  accompanied  by  uneasiness, 
by  a  sense  of  constriction,  or  of  weight  or  pain  in  the  region ' 
of  the  heart,  and  by  a  sense  of  sinking,  or  fluttering  in  the 
epigastrium.  Sometimes,  extreme  dyspnoea  and  headache, 
vertigo,  and  ringing  in  the  ears  are  present.  At  other  times, 
none  of  these  symptoms  are  observed,  and  the  palpitation 
is  the  only  symptom  we  are  called  upon  to  treat. 

DIFFERENTIAL  DIAGNOSIS. — To  distinguish  between  car- 
diac palpitation  independent  of  organic  disease  of  the  heart, 
and  cardiac  palpitation  depending  upon  organic  cardiac 
disease,  is  of  the  greatest  importance. 

Cardiac  palpitation  independent  of  cardiac  disease  comes 
on  suddenly  and  is  not  constant,  whereas  organic  cardiac 
palpitation  comes  on  slowly  and  is  constant.  In  inorganic 
palpitation  of  the  heart,  all  the  physical  signs  of  organic 
cardiac  disease  are  absent.  In  inorganic,  cynosis  is  never 
present,  while  it  is  a  frequent  attendant  of  organic. 
Patients  free  from  organic  heart  disease  complain  more  fre- 
quently of  palpitation  than  those  having  organic  cardiac 
disease.  Organic  palpitation  is  increased  by  exercise, 
while  inorganic  is  increased  by  a  sedentary  life. 

PROGNOSIS. — In  cardiac  palpitation  independent  of  or- 
ganic heart  disease,  the  prognosis  is  always  good  ;  although 
it  may  cause  the  patient  great  uneasiness,  it  never  destroys 
life. 

TREATMENT, — In  the  treatment  of  each  case  of  nervous 
cardiac  palpitation,  to  find  out  and  remove  its  cause  is  of 
first  importance.  In  anaemic  patients,  iron  is  often  of  signal 
service.  Treatment  of  some  form  of  uterine  derangement 
will  frequently  relieve  hysterical  palpitation.  If  the  exces- 
sive use  of  alcoholic  stimulants,  tobacco,  or  strong  tea  and 
coffee,  causes  it,  their  use  must  be  discontinued.  Occurring 
in  a  gouty  subject,  those  means  which  have  been  found  to 
relieve  gouty  manifestations  must  be  employed. 

Those  in  whom  no  special  cause  for  the  palpitation  can  be 
found,  should  be  directed  to  sponge  the  surface  of  the  body 
night  and  morning  in  cold  water  ;  to  exercise  moderately  in 


CAEDIAC   PALPITATION.  425 

the  open  air ;  and  they  should  be  forbidden  luxurious 
living  and  all  violent  physical  exertion,  especially  running. 

During  the  attacks,  relief  will  usually  be  obtained  by  the 
administration  of  some  of  the  more  reliable  nervines  and 
diffusible  stimulants.  Narcotics  generally  do  harm.  Digi- 
talis should  never  be  given  in  purely  nervous  cardiac  palpi- 
tation. 

A  very  important  element  in  the  successful  management 
.  of  an  attack  of  nervous  cardiac  palpitation,  is  the  positive 
assurance  of  the  medical  attendant  that  there  is  no  danger 
attending  the  paroxysm. 

ANGINA  PECTORIS. 

Angina  pectoris  may  be  regarded  as  a  neurosis  of  the 
heart,  due  to  organic  changes  in  its  structure.  Although, 
strictly  speaking,  it  must  be  regarded  as  a  symptom,  or  a 
collection  of  symptoms,  of  organic  cardiac  disease  of  long 
standing,  and  not  a  distinct  affection,  yet  it  will  be  neces- 
sary for  me  to  give  it  a  separate  consideration,  as  by  medical 
writers  it  has  come  to  be  regarded  as  a  distinct  disorder. 

MORBID  ANATOMY. — There  is  no  form  of  cardiac  or  aortic 
disease  with  which  angina  pectoris  has  not  been  found  asso- 
ciated, and  there  is  no  form  with  which  it  is  invariably  or 
even  generally  present.  There  are,  however,  two  forms  of 
heart  disease  with  which  it  is  especially  liable  to  occur, 
namely,  obstruction  to  the  coronary  circulation,  and  fatty  de- 
generation of  the  muscular  tissue  of  the  heart.  The  other 
diseased  states  with  which  it  is  specially  liable  to  occur  are, 
insufficiency  of  the  aortic  valves,  with  a  rigid  dilated  state 
of  the  ascending  portion  of  the  arch  of  the  aorta,  com- 
bined with  dilatation  of  the  left  ventricle.  When  these 
diseased  states  exist,  angina  pectoris  will  not  occur  unless 
the  heart's  action  is  suddenly  disturbed,  or  its  movements 
impeded  by  some  mechanical  cause.  Some  claim  that  the 
addition  of  a  nervous  element  is  necessary,  and  that  the 
nervous  element  has  its  seat  in  the  pneumogastric  or  car- 
diac plexus,  which  gives  rise  to  cardiac  spasm.  It  is  doubt- 
ful whether  it  is  in  any  way  connected  with  cardiac  spasm 
or  neuralgia. 


426  SYMPTOMS. 

ETIOLOGY. — The  predisposing  causes  of  angina  pectoris 
have  been  sufficiently  considered  in  connection  with  its 
morbid  anatomy.  Its  exciting  causes  are  mental  emotions, 
prolonged  physical  exertion,  errors  of  diet,  and  anything 
which  has  a  tendency  to  disturb  the  heart' s  action. 

SYMPTOMS. — The  symptoms  which  attend  an  attack  of 
angina  pectoris  are  quite  characteristic.  The  patient  is  sud- 
denly seized  with  an  intense  agonizing  pain  in  the  precordial 
region,  shooting  through  to  the  back  and  along  the  left 
arm.  This  pain  is  of  a  stabbing  or  lancinating  character, 
and  produces  a  sensation  of  intense  oppression  or  impend- 
ing suif ocation — a  feeling  as  though  death  was  near  at  hand. 
At  the  commencement  of  this  pain  his  countenance  becomes 
deadly  pale,  and  is  expressive  of  extreme  anxiety  and  suf- 
fering ;  the  surface  is  covered  with  a  cold  perspiration,  the 
pulse  falters,  and  may  be  almost  imperceptible,  the  respi- 
ration is  short  and  hurried,  the  face  livid,  and  he  is  unable 
to  lie  down  or  even  to  move,  for  the  least  motion  aggravates 
his  sufferings.  His  consciousness  is  undisturbed,  and  his 
spinal  as  well  as  his  cerebral  functions  are  unaffected.  Not 
unfrequently  the  rhythm  of  the  heart's  action  is  undisturbed, 
and  the  patient  does  not  even  experience  palpitation. 
Sometimes  the  action  of  the  heart  is  so  much  deranged  that 
syncope  or  even  sudden  death  occurs.  Usually,  after  a  few 
moments,  or  at  the  longest,  half  an  hour,  the  paroxysm 
gradually  subsides.  At  first  there  are  long  intervals  be- 
tween these  attacks,  but  afterward  they  become  of  frequent 
occurrence.  Between  the  attacks  the  health  may  be  un- 
impaired ;  in  many  cases,  evidences  of  extensive  disease  of 
the  heart  may  be  detected. 

DIFFERENTIAL  DIAGNOSIS. — Angina  pectoris  may  be  con- 
founded with  spasmodic  asthma,  hysteria,  intercostal  neu- 
ralgia, myalgia,  and  the  first  stage  of  acute  pleurisy. 
Although  the  visible  phenomena  attending  a  paroxysm  of 
angina  pectoris  may  bear  a  striking  resemblance  to  those  of 
spasmodic  asthma,  a  physical  examination  of  the  chest  will 
detect  the  presence  or  absence  of  the  characteristic  physical 
signs  of  the  asthma,  and  thus  lead  you  to  a  correct  diag- 
nosis. 


ANGINA  PECTOEIS.  427 

The  intermitting  and  irregular  character  of  the  pulse  in 
angina  pectoris  will  enable  you  to  distinguish  it  from  a 
hysterical  paroxysm.  In  intercostal  neuralgia  the  duration 
of  the  attack,  the  points  of  tenderness,  the  direction  of  the 
pain,  and  the  absence  of  cardiac  disturbance,  will  enable 
you  to  distinguish  it  from  angina  pectoris.  Myalgia  and 
acute  pleurisy  may  simulate  angina  pectoris.  In  each, 
acute  pain  and  catching  breath  are  present ;  but  the  condi- 
tion of  the  circulation,  taken  in  connection  with  the  locality 
of  the  pain,  and  the  physical  signs  of  pleurisy,  will  gener- 
ally decide  the  question. 

PROGNOSIS. — The  prognosis  in  angina  pectoris  necessarily 
is  unfavorable.  Sometimes  the  first  attack  proves  fatal ;  in 
more  instances  the  second  or  third,  while  in  many  more, 
perhaps  in  the  majority  of  instances,  the  patient  at  irregular 
intervals  experiences  a  succession  of  attacks,  and  each 
paroxysm  is  more  severe  than  the  previous  one,  until 
finally,  after  a  period  extending  from  one  to  six  or  eight 
years,  an  attack  occurs  in  which  the  heart's  action  is 
arrested,  and  death  ensues. 

TREATMENT. — During  an  attack  of  angina  pectoris,  means 
should  be  employed  to  alleviate  or  arrest  the  paroxysm ; 
during  the  interval  we  should  endeavor,  if  possible,  to 
remove  the  exciting  cause,  or  lessen  its  predisposing  power. 

It  is  doubtful  whether  there  are  any  remedial  agents  that 
have  the  power  to  arrest  or  very  greatly  relieve  a  paroxysm. 
Diffusible  stimulants,  sedatives,  and  anti-spasmodics  have 
all  been  employed,  but  so  far  as  my  experience  goes,  they 
have  no  power  to  alleviate  or  arrest  the  paroxysm.  Rest, 
and  the  free  administration  of  digitalis,  are  of  the  greatest 
service.  Opiates,  chloroform,  nitrate  of  amyle,  and  other 
narcotics,  should  not  be  used. 

During  the  interval,  all  violent  emotions  and  all  active 
physical  exercise  must  be  avoided.  Indigestion,  flatulence, 
and  everything  which  shall  embarrass  the  heart's  action, 
must  be  guarded  against,  and  when  present  should  be 
relieved  by  careful  attention  to  the  diet. 

The  only  medicinal  remedies  which  I  have  found  of  ser- 
vice in  delaying  and  rendering  less  severe  the  paroxysm  of 


428  TKEATMENT. 

angina  pectoris,  are  iron,   strychnine,   and  arsenic  ;   these 
should  be  daily  administered  in  small  doses. 

When  angina  pectoris  is  associated  with  fatty  heart,  the 
rules  given  for  the  management  of  the  latter  disease  should 
be  observed. 


DISEASES    OF   THE   KIDNEYS. 


LECTURE  XXXVI. 


DISEASES  OP  THE  KIDNEYS. 

Introduction. — Renal  Congestion. — Renal  Hemorrhage. 

G-EISTTLEMEN" : — The  close  relationship  existing  between 
diseases  of  the  kidneys  and  the  different  forms  of  disease  of 
the  heart  and  lungs  which  have  been  engaging  our  atten- 
tion, is  a  sufficient  reason  for  considering  these  three  classes 
of  disease  in  succession. 

You  will  very  rarely  meet  with  any  form  of  chronic 
kidney  disease  that  is  not  associated  with  some  lesion  of 
the  heart  or  lungs  ;  and  all  the  various  diseases  of  the  heart 
and  lungs  which  we  have  been  considering,  may  be  com- 
plicated by  changes  or  lesions  in  the  kidney.  There  seems 
to  be  a  necessarily  intimate  relation  existing  between  these 
three  forms  of  disease — so  intimate,  that  for  a  proper  under- 
standing of  the  symptoms  of  one,  a  certain  amount  of  knowl- 
edge concerning  the  others  is  necessitated. 

Without  an  exact  knowledge  of  the  normal  circulation, 
minute  anatomical  structure  and  functions  of  the  kidney, 
it  is  impossible  for  one  to  understand  either  the  causation, 
morbid  anatomy,  or  symptoms  of  the  different  forms  of 
renal  disease. 

It  will  not  be  necessary  for  me  at  this  time  to  dwell  upon 
any  of  these  anatomical  or  physiological  points,  for  the 
reason  that  your  teacher  of  physiology  and  histology  has 
very  recently  thoroughly  taught  you  concerning  them,  and 
later  text-books  on  physiology  enter  very  fully  into  the 
discussion  of  them.  My  allusions  to  the  minute  anatomy 


432  EENAL   CONGESTION. 

and  functions  of  the  kidney  will  be  such  as  I  might  make 
if  together  we  had  just  studied  this  subject. 

It  is  not  necessary  for  me  to  enter  into  any  argument  to 
prove  that  this  is  the  most  important  class  of  diseases 
which  as  medical  or.  surgical  practitioners  you  will  be  called 
upon  to  treat.  The  large  number  of  special  treatises  on 
this  class  of  diseases,  which  have  been  issued  within  the 
last  ten  years,  is  sufficient  evidence  of  their  importance. 

I  shall  consider  diseases  of  the  kidneys  under  the  follow- 
ing heads : 

First.  —RENAL  CONGESTION. 

Second. — RENAL  HEMORRHAGE  (including  infarctions). 

Third. — BRIGHT' s  DISEASES. 

Fourth .  — P  YELITIS  . 

Fifth. — HYDRONEPHROSIS. 

Sixth. — CYSTIC  KIDNEYS. 

Seventh. — PRECIPITATES  AND  CONCRETIONS  (renal  cal- 
culi). 

Eighth. — NEW  GROWTHS  (cancer,  etc.). 

Ninth. — PARASITES. 

The  most  important  of  this  list  of  diseases,  and  those 
which  will  chiefly  engage  our  attention,  are  Bright' s  diseases 
of  the  kidneys. 

I  shall  now  invite  your  attention  to  the  first  in  the  list, 
which  is  renal  congestion. 

RENAL   CONGESTION. 

Renal  congestion,  or,  as  it  is  sometimes  called,  hypenemia 
of  the  kidneys,  may  be  active  or  passive  ;  passive  renal 
congestion  may  also  be  termed  mechanical.  These  two 
forms  of  congestion  differ  very  materially. 

MORBID  ANATOMY. — In  active  renal  congestion,  usually 
you  will  find  the  kidney  very  much  increased  in  size.  The 
congestion  may  have  its  seat  in  the  cortical  or  medullary 
portion,  and  may  be  much  more  marked  in  one  portion  than 
in  another.  In  all  instances  the  congestion  is  more  marked 
at  the  base  of  the  pyramids. 

Kidneys  that  are  the  seat  of  active  congestion  are  not  only 
increased  in  size,  but  they  are  of  an  unnaturally  dark  color, 


MORBID   ANATOMY.  433 

the  capsule  is  non-adherent,  their  surface  is  smooth,  and 
the  organs  are  softer  and  moister  than  natural.  Upon  sec- 
tion, you  will  notice  dark  points  scattered  over  the  cut  sur- 
face ;  these  dark  points  correspond  to  the  Malpighian  tufts, 
sometimes  they  represent  spots  of  minute  ecchymosis.  A 
more  or  less  abundant  dark  fluid  follows  the  section  ;  this 
dark  fluid  is  partly  serum  and  partly  blood,  for  there  is  al- 
ways more  or  less  oedema  of  the  kidneys  accompanying  ac- 
tive congestion.  In  active  renal  congestion  the  congestion 
mainly  occurs  in  the  renal  arteries,  and  in  the  Malpighian 
tufts  before  reaching  the  veins  of  the  kidneys. 

When  kidneys,  which  are  the  seat  of  active  congestion, 
are  microscopically  examined,  it  is  found  that  all  the 
changes  are  simply  due  to  an  engorgement  of  the  blood-ves- 
sels, and  an  infiltration  of  serum  into  the  intertubular  struc- 
ture ;  the  infiltration  into  the  intertubular  structure  may  be 
slight  or  considerable.  This  form  of  congestion  is  usually 
most  marked  in  the  cortical  portion  of  the  kidneys. 

In  passive  or  mechanical  renal  congestion,  particularly  in 
that  form  which  occurs  in  chronic  cardiac  disease,  the  kid- 
neys are  not  very  much  increased  in  size,  but  they  have  a 
stony  hardness  which  is  quite  characteristic.  Their  surface 
is  smooth,  their  capsules  non-adherent,  and  they  are  of  a 
uniform  red  color.  They  have  a  firmness  which  is  never 
noticed  in  any  other  form  of  kidney  change. 

Upon  section,  it  will  be  noticed  that  the  medullary  portion 
is  of  a  darker  color  than  the  cortical  portion.  The  cortical 
portion  has  streaks  of  red  color  rather  than  a  uniform  con- 
gestion. The  Malpighian  tubes  are  not  prominent,  they  are 
simply  filled  with  blood,  but  not  intensely  engorged  as  is 
the  case  in  active  congestion.  The  veins  of  the  kidney  are 
dilated,  sometimes  very  extensively,  and  the  hardness  of 
the  organ  is,  undoubtedly,  to  a  great  extent,  due  to  a  con- 
stant dilated  condition  of  the  efferent  capillary  vessels.  In 
either  of  these  conditions,  either  active  or  passive  congestion 
of  the  kidneys,  there  is  necessarily  no  inflammatory  changes. 

In  passive  renal  congestion  the  epithelium  of  the  convo- 
luted tubes  may  have  a  peculiar  stiff  appearance,  but  this  is 

not  the  result  of  an  inflammatory  process. 
28 


434  RENAL   CONGESTION. 

Both  of  these  forms  of  congestion  may  lead  to,  or  be  ac- 
companied by  inflammation  of  the  uriniferous  tubes,  and 
they  may  both  exist  without  any  inflammatory  changes. 
In  most  instances,  when  a  kidney  is  the  seat  of  extensive 
passive  congestion,  there  will  be  more  or  less  change  in  the 
tubules  characteristic  of  simple  catarrh.  It  is  only  a  step 
from  passive  congestion  to  catarrh  of  the  uriniferous  tubes. 

If  you  have  an  inflammation  established  from  active  con- 
gestion, it  will  not  be  catarrhal  in  its  nature.  If  it  occurs 
in  connection  with  passive  congestion,  it  will  always  be 
catarrhal. 

ETIOLOGY. — The  causes  of  renal  congestion  are  numerous, 
and  those  which  produce  active  congestion  are  very  different 
from  those  which  produce  passive  congestion. 

Active  renal  congestion  may  be  produced  by  exposure  of 
the  body  to  sudden  changes  in  temperature,  and  by  any  of 
those  blood-poisons  which  give  rise  to  infectious  disease, 
such  as  scarlatina,  diphtheria,  typhus  fever,  etc.  It  may  also 
be  produced  by  malaria,  and  is  sometimes  a  prominent  fea- 
ture of  a  violent  malarial  paroxysm  ;  again,  it  may  be  pro- 
duced by  a  prolonged  and  excessive  use  of  certain  agents 
which  give  rise  to  irritation  of  the  urinary  passages,  such  as 
cantharides,  turpentine,  nitre,  capaiba,  etc. 

The  irritating  state  of  the  urine  in  diabetes  and  cholsemia 
may  also  cause  renal  congestion.  Morbid  formation  in  the 
kidney  and  the  early  stage  of  inflammation  are  frequently 
attended  by  active  renal  congestion. 

Passive  renal  congestion  occurs  in  connection  with  any 
disease  of  the  heart  or  lungs,  or  any  mechanical  obstruction 
in  the  thorax  or  abdominal  cavities  which  interferes  with 
the  passage  of  venous  blood  into  the  right  auricle,  or  of  ar- 
terial blood  from  the  left  ventricle.  All  valvular  lesions  of 
the  heart,  or  structural  diseases  of  the  cardiac  walls,  which 
interfere  with  venous  return,  come  under  this  head,  as  well 
as  all  those  forms  of  pulmonary  disease  which  interfere  with 
the  pulmonary  circulation,  as  emphysema,  pleuritic  effu- 
sion, etc.  Passive  renal  congestion  may  also  be  due  to 
pressure  on  the  emulgent  renal  veins,  or  inferior  cava  in 
pregnancy,  and  when  abdominal  tumors  are  present.  In 


SYMPTOMS.  435 

aortic  diseases  it  is  not  because  the  renal  arteries  do  not  re- 
ceive sufficient  blood,  but  because  there  is  a  delay  in  the 
venous  circulation  that  passive  congestion  is  developed. 

SYMPTOMS. — Almost  the  only  symptoms  that  attend  the 
different  forms  and  degrees  of  renal  congestion  are  confined 
to  changes  in  the  urine  ;  in  fact  it  cannot  be  recognized  ex- 
cept by  these  urinary  changes.  There  are  no  constant  ob- 
jective symptoms  which  attend  its  occurrence.  It  is  rarely 
if  ever  attended  by  pain,  for  the  sensitive  nerves  of  the  kid- 
ney are  not  sufficiently  numerous  to  permit  this  condition 
to  cause  pain,  nor  has  it  any  other  independent  objective 
phenomena. 

Clinically,  renal  congestion  is  marked  by  a  decrease  in 
the  quantity  of  the  urine,  with  an  increase  in  its  specific 
gravity ;  it  usually  contains  a  moderate  amount  of  albumen 
and  some  traces  of  blood. 

The  simultaneous  appearance  of  blood  and  albumen  in 
the  urine  is  so  usual  in  congestion  of  the  kidneys,  that  the 
appearance  of  albumen  alone,  without  a  trace  of  blood, 
almost  excludes  renal  congestion  from  the  diagnosis. 

If  albumen  alone  is  present,  you  have  good  reason  for 
the  belief  that  its  presence  is  due  to  inflammatory  processes 
and  not  to  simple  congestion. 

Sometimes  the  blood  is  sufficient  in  quantity  to  be  seen 
in  the  form  of  blood-casts  in  the  urine,  but  this  is  not  usual 
in  simple  congestion.  It  is  possible  to  have  blood-casts  of 
the  uriniferous  tubes  in  simple  renal  congestion  without 
inflammation,  but  it  is  not  common. 

The  effect  of  renal  congestion  depends  upon  how  far  the 
suppression  of  urine  may  extend  as  the  result  of  the  con- 
gestion. 

The  differential  diagnosis  of  renal  congestion  will  be 
considered  in  connection  with  the  history  of  the  different 
forms  of  Bright' s  disease. 

PROGNOSIS.—  The  prognosis  in  renal  congestion,  when  the 
exciting  cause  is  of  a  transient  character,  is  good.  Unques- 
tionably, passive  renal  congestion,  such  as  occurs  in  the 
advanced  stages  of  cardiac  disease,  has  very  much  to  do 
with  weakening  or  destroying  the  vitality  of  the  patient, 


436  EEXAL   CONGESTION. 

and  placing  him  in  a  condition  favorable  to  the  occurrence 
of  sudden  death ;  but  rarely,  if  ever,  does  it  directly 
destroy  life. 

That  form  of  active  renal  congestion  which  occurs  in  con- 
nection with  congestive  malarial  fevers  in  hot  climates,  is 
sometimes  so  intense  as  to  entirely  arrest  the  functions  of 
the  kidneys,  and  becomes  the  direct  cause  of  death.  Under 
such  circumstances,  it  is  usually  accompanied  by  extensive 
renal  hemorrhage. 

In  cases  of  renal  congestion,  either  active  or  passive,  you 
should  constantly  bear  in  mind  that  there  is  great  danger 
that  the  congestion  may  lead  to,  or  be  followed  by  inflam- 
mation of  the  uriniferous  tubes  or  the  intertubular  struc- 
ture, and  the  consequent  development  of  Bright' s  disease  of 
the  kidneys. 

TREATMENT. — The  most  important  thing  to  be  accom- 
plished in  the  treatment  of  active  renal  congestion,  is  to 
find  out  and  as  quickly  as  possible  remove  its  cause.  The 
treatment  is  to  be  addressed  to  the  kidneys.  First,  place 
the  patient  in  bed  in  a  room  with  a  temperature  above  75°  F.  ; 
then  apply  a  dozen  dry  or  wet  cups  over  the  lumbar  region. 
Let  the  patient  drink  freely  of  diluent  drinks,  administer 
one  or  two  drastic  purgatives.  Induce  moderate  diapho- 
resis and  carefully  avoid  all  stimulants. 

By  the  adoption  of  these  measures  you  may  expect  in 
most  cases  to  very  speedily  relieve  the  renal  congestion,  and 
restore  the  kidney  to  the  performance  of  its  normal  function. 

In  passive  renal  congestion,  if  counter-irritation  is  em- 
ployed at  all,  it  must  be  mild  in  character,  such  as  three 
or  four  dry  cups,  or  some  form  of  embrocation  over  the 
lumbar  region  ;  severe  remedies  of  this  kind  are  to  be 
avoided,  especially  blisters.  The  intestines  may  occasion- 
ally be  unloaded  by  a  brisk  cathartic  ;  an  occasional  dose 
of  calomel,  in  combination  with  some  other  purgative,  will 
be  of  service. 

Occurring  as  it  does  in  the  great  majority  of  instances 
in  connection  with  some  chronic  cardiac  lesion,  the  remedial 
agent  which  will  be  found  most  serviceable  is  digitalis. 

Failure  of  heart-power  is  generally  the  precursor  of  pas- 


MOEBID   ANATOMY.  437 

sive  renal  congestion  ;  under  such  circumstances  the  digi- 
talis is  the  most  reliable  agent  for  increasing  the  heart- 
power,  and  thus  regulating  the  circulation  of  the  kidney. 
If  the  evidences  of  the  passive  congestion  indicate  that 
there  is  great  disturbance  of  the  renal  function,  the  digitalis 
must  be  administered  freely  until  relief  is  obtained. 

When  the  obstruction  to  the  renal  circulation  is  directly 
mechanical,  as  in  pregnancy,  and  in  fluid  accumulation  in 
the  abdominal  cavity,  much  may  be  accomplished  by  change 
of  position  of  the  patient,  in  removing  or  relieving  the 
pressure  on  the  abdominal  venous  circulation. 

In  connection  with  pregnancy,  the  application  of  cups  to 
the  lumbar  region  is  essential. 


RENAL  HEMORRHAGE. 

I  will  now  pass  from  renal  congestion  to  renal  hemor- 
rhage. 

The  two  conditions  are  very  liable  to  be  associated.  In 
connection  with  extensive  renal  congestion  of  an  active 
character,  there  is  frequently  more  or  less  extensive  renal 
hemorrhage. 

MOEBID  ANATOMY.  —  The  anatomical  changes  that  occur 
in  a  kidney  which  is  the  seat  of  renal  hemorrhage,  do  not 
differ  essentially  from  that  already  described  as  marking 
the  presence  of  renal  congestion,  unless  the  hemorrhage  is 
due  to  the  occurrence  of  hemorrhagic  infarction  or  renal 
calculi.  Blood  may  be  diffused  into  the  uriniferous  tubules 
or  the  interstitial  tissue,  giving  rise  to  ecchymotic  spots 
varying  in  size,  from  which,  when  cut  into,  blood  freely 
flows. 

The  most  frequent  spontaneous  renal  hemorrhage  is  tha,t 
which  occurs  in  connection  with  the  occurrence  of  renal 
embolism  and  infarction.  Its  occurrence  is  marked  by  the 
development  of  hard,  uniform  masses  in  the  cortical  por- 
tion of  the  kidney  ;  these  masses  are  usually  wedge-shaped, 
and  have  their  sharp  edges  toward  the  hilus  of  the  kidney 
and  their  base  toward  the  surface. 

They  vary  in  size  according  to  the  size  of  the  vessel  ob-  . 


438  RE^AL  HEMORRHAGE. 

structed ;  they  may  be  capillary,  and  they  are  of  very 
small  size.  These  infarctions  when  first  formed  are  of  a 
dark  red  color,  and  are  as  firm  as  normal  kidney  tissue ; 
very  soon  after  their  formation  they  begin  to  change  in 
color ;  they  soon  lose  their  dark  red  hue,  become  of  a 
lighter  color,  and  their  centres  present  very  much  the 
appearance  of  a  cheesy  material ;  sometimes  they  undergo 
cheesy  change,  which  always  begins  at  the  centres. 

Around  these  infarctions  a  zone  of  redness  is  formed,  but 
that  zone  is  beyond  the  infarction  in  the  normal  kidney 
tissue.  A  congestion  takes  place  in  vessels,  from  changes 
occurring  in  the  uriniferous  tubes  attached  to  the  capillaries 
in  that  portion  of  the  kidney  which  surrounds  the  infarction  ; 
there  is  also  more  or  less  rapid  production  of  lymphoid  cells 
in  this  surrounding  zone.  If  the  infarction  does  not  disap- 
pear by  absorption,  this  zone-change  continues  until  there 
is  more  or  less  of  cicatricial  tissue  developed  about  the  in- 
farction ;  the  infarction  shrinks  in  consequence  of  the  con- 
traction of  the  tissue,  gradually  becoming  less  and  less,  and 
after  a  time  disappears  altogether,  leaving  only  cicatricial 
tissue  to  mark  its  former  site.  On  the  other  hand,  the  pro- 
duction of  lymphoid  elements  may  be  rapid  and  abundant, 
until  the  entire  mass  may  undergo  purulent  transformation, 
producing  abscesses  which  will  occupy  the  seat  of  the  infarc- 
tion. This  is  one  of  the  ways  in  which  abscesses  are  formed 
in  the  kidneys. 

Again,  these  infarctions  may  undergo  a  still  more  rapid 
degeneration,  increasing  in  size  and  becoming  necrotic,  so 
that  at  the  autopsy  a  gangrenous  mass  is  found,  as  the 
result  of  the  necrotic  change  which  has  taken  place  in  the 
infarction. 

Again,  there  may  be  little  masses  found  scattered  through- 
out the  substance  of  the  kidney,  especially  the  cortical  por- 
tion, looking  very  much  like  ecchymotic  spots,  which  are 
simply  capillary  thrombi — these  are  usually  due  to  some 
slowing  of  the  circulation  in  the  capillary  vessels.  These 
capillary  thrombi  may  be  very  numerous,  and  they  may 
undergo  changes  similar  to  the  larger  infarctions.  At 
your  post-mortem  examination  you  may  find  the  kidneys 


ETIOLOGY.  439 

studded  all  over  with  minute  abscesses ;  unquestionably, 
these  little  collections  of  pus  are  nothing  more  than  minute 
capillary  infarctions  or  thrombi,  which  have  undergone 
transformation  into  little  abscesses.  Thus  we  may  have  a 
single  abscess  or  many  abscesses  of  the  kidneys  occurring  as 
the  result  of  infarctions.  In  connection  with  the  development 
of  these  infarctions  you  may  have  congestion  of  the  kidneys 
as  already  described.  In  the  passive  form  of  renal  conges- 
tion you  are  especially  liable  to  have  this  form  of  renal 
hemorrhage  occur. 

ETIOLOGY. — Intense  active  congestion  of  the  kidney  is  one 
cause  of  renal  hemorrhage.  It  is  possible  for  the  kidneys 
to  become  so  engorged  with  blood  as  to  give  rise  to  intense 
renal  congestion  and  thus  cause  renal  hemorrhage  ;  such 
an  occurrence  is  exceedingly  rare  ;  some  deny  the  possibility 
of  its  occurrence. 

Renal  hemorrhage  may  also  be  the  result  of  injuries. 
The  most  common  form  of  such  hemorrhage  is  that  which 
occurrs  in  connection  with  renal  calculi  in  the  pelvis  of  the 
kidneys,  wounds,  contusions,  etc. 

Again,  renal  hemorrhage  may  occur  as  the  result  of  in- 
tense renal  congestion  and  rupture  of  the  overloaded  renal 
capillaries,  in  connection  with  the  first  stage  of  acute  inflam- 
mation of  the  kidneys,  such  as  is  sometimes  met  with  in 
scarlet  fever,  typhus,  and  malarial  fevers,  and  in  other 
infectious  diseases. 

Renal  hemorrhage  may  also  occur  as  the  result  of  new 
formations,  and  is  especially  liable  to  occur  in  connection 
with  cancerous  developments  of  the  kidney. 

Blood  changes,  such  as  occur  in  purpura,  scurvy,  etc., 
may  cause  renal  hemorrhage. 

Passive  obstructive  congestion  from  cardiac  diseases  may 
become  so  intense  as  to  give  rise  to  renal  hemorrhages. 

Then  again,  you  may  have  renal  hemorrhage  from  infarc- 
tion due  to  renal  embolism  or  capillary  thrombosis. 

SYMPTOMS. — There  are  no  very  constant  or  distinctive 
objective  symptoms  of  renal  hemorrhage.  Our  knowledge 
of  its  occurrence  during  life  rests  almost  altogether  upon 
the  results  of  the  examination  of  the  urine.  You  will  not 


440  KEl^AL   HEMOKKHAGE. 

be  able  to  recognize  the  existence  of  any  of  the  varieties 
of  renal  hemorrhage,  unless  the  blood  is  effused  into  the 
uriniferous  tubules  or  into  the  hilus  of  the  kidney  and  dis- 
charged in  the  urine.  At  autopsies  you  will  frequently  find 
large  infarctions  of  the  kidney,  which  during  life  have 
given  no  indication  of  their  existence,  because  there  was  no 
rupture  into  the  uriniferous  tubules,  no  extravasation  of 
blood,  consequently  no  blood  was  found  in  the  urine. 

The  course  of  a  renal  hemorrhage  depends  to  a  great  ex- 
tent upon  the  cause  which  produces  it.  When  dependent 
upon  the  presence  of  a  renal  calculi,  the  hemorrhage  occurs 
regularly  after  every  violent  exertion.  When  it  arises  from 
cancer  or  other  tumors,  it  is  generally  profuse  and  persist- 
ent. The  bleeding  which  accompanies  inflammation  of  the 
kidneys  in  the  infectious  diseases  is  never  severe  nor  con- 
stant ;  it  may  be  so  slight  as  only  to  be  recognized  by  a 
microscopical  examination  of  the  urine. 

That  form  of  renal  hemorrhage  which  occurs  in  the 
malarial  districts  of  hot  climates,  is  usually  profuse  and 
occurs  periodically. 

When  renal  infarction  is  accompanied  by  hsematuria,  the 
patient  is  usually  seized  with  a  chill  on  the  occurrence  of 
the  infarction,  followed  by  some  pain  in  the  back,  and  more 
or  less  nausea  and  vomiting.  If,  therefore,  these  symptoms 
are  developed  in  connection  with  cardiac  disease  or  pysemia, 
you  may  be  almost  certain  that  renal  infarctions  have 
occurred. 

PROGNOSIS. — The  prognosis  in  renal  hemorrhage  depends 
upon  the  conditions  and  circumstances  under  which  the 
hemorrhage  occurs.  If  it  occurs  in  connection  with  renal 
calculi  or  cancerous  disease  of  the  kidney,  the  prognosis  is 
bad,  life  is  endangered  under  these  circumstances  from  the 
exhaustion  produced  by  the  continued  loss  of  blood. 

Renal  hemorrhage  occurring  in  connection  with  infectious 
disease  has  no  particular  significance  ;  it  merely  is  an  indica- 
tion of  intense  renal  hypersemia. 

When  you  have  reason  to  believe  that  a  hemorrhagic 
infarction  has  occurred  in  the  kidney,  its  occurrence  must 
always  be  regarded  as  attended  with  danger  to  life,  not  that 


TEEATMENT.  441 

it  is  necessarily  fatal,  or  that  the  prognosis  is  necessarily 
unfavorable ;  but  the  fact  that  infarctions  exist  will  cause 
anxiety  as  to  the  development  of  the  other  degenerative 
changes  in  the  kidneys,  to  which  reference  has  already  been 
made. 

TREATMENT. — The  first  thing  to  be  accomplished  in  the 
treatment  of  a  case  of  renal  hemorrhage  is  to  find  out,  and, 
if  possible,  remove  its  cause.  In  many  cases  where  the 
main  disease  is  amenable  to  treatment,  the  renal  hemorrhage 
does  not  require  any  special  attention. 

During  the  occurrence  of  the  hemorrhage,  the  patient 
should  be  kept  absolutely  at  rest.  If  there  is  danger  of 
exhaustion  from  repeated  and  profuse  hemorrhages,  ice- 
bags  may  be  applied  to  the  lumbar  region,  and  styptics  ad- 
ministered internally.  The  remedial  agent  which  seems  to 
have  the  greatest  control  over  these  hemorrhages  is  tannic 
acid,  it  being  expelled  from  the  system  through  the  kidneys 
in  the  form  of  gallic  acid ;  a  powerful  astringent  is  thus 
brought  directly  in  contact  with  the  uriniferous  tubes  and 
urinary  passages.  Ergot  may  sometimes  be  of  service  when 
administered  in  large  doses. 

If  the  hemorrhage  arises  in  connection  with  the  develop- 
ment of  malarial  poisoning,  large  doses  of  quinine  are  in- 
dicated. 

The  danger  from  acute  renal  inflammation  must  always 
be  borne  in  mind  when  renal  hemorrhage  occurs  in  connec- 
tion with  the  infectious  diseases ;  the  proper  measures  for 
the  subduing  or  arresting  of  such  inflammations  must  be 
promptly  resorted  to. 


LECTURE    XXXVII. 


ACUTE  URAEMIA. 

Ursemic  Convulsions. — Uraemic  Coma. 

BEFOKE  commencing  the  history  of  those  diseases  of  the 
kidneys  which  are  usually  included  under  the  general  term 
of  Bright' s  diseases,  I  shall  invite  your  attention  to  the 
subject  of  acute  uraemia. 

Under  this  term  may  be  grouped  two  classes  of  symp- 
toms, which  differ  in  their  mode  of  development  and  in 
their  attendant  phenomena. 

In  the  one,  nausea,  vomiting,  and  headache  usher  in 
twitchings  and  epileptiform  convulsions  of  the  voluntary 
muscles,  a  state  which  has  received  the  name  of  urcemic 
convulsions.  In  the  other,  headache  and  drowsiness,  or 
convulsions,  usher  in  a  state  of  insensibility  which  has 
received  the  name  of  urcsm/'c  coma. 

The  primary  cause  of  both  these  conditions  is  always  to 
be  found  in  a  failure  of  the  kidneys  to  perform  their  normal 
function  of  elimination,  and  the  consequent  accumulation 
in  the  circulation  of  some  or  all  the  poisonous  elements  of 
the  urine. 

This  condition  may  occur  in  the  course  of  any  disease  in 
which  suppression  of  the  renal  secretion  takes  place ;  such 
arrest  of  the  function  of  the  kidneys  most  frequently  occurs 
in  scarlatina,  in  the  different  forms  and  stages  of  Bright' s 
disease,  in  the  puerperal  state,  and  in  connection  with  the 
surgery  of  the  urethra. 

ETIOLOGY. — A  number  of  theories  have  been  advanced  in 
regard  to  the  exact  element  which  acts  as  the  poisonous 
agent  in  uraemia. 


ETIOLOGY.  443 

The  earliest  accepted  view  is  that  which  attributes  the 
symptoms  of  uraemia  to  retained  urea.  Although  this 
view  at  different  times  has  been  discarded  and  apparently 
disproved  by  the  experiments  of  distinguished  observers, 
to-day  it  is  the  view  received  by  most  authors. 

Some  years  since  the  theory  was  advanced  that  urea  as 
urea,  is  innocuous,  and  that  the  poisonous  agent  was  car- 
bonate of  ammonia,  resulting  from  decomposition  in  the 
blood  of  urea  into  carbonate  of  ammonia  and  water,  which 
decomposition  was  ascribed  to  the  action  of  a  ferment  in  the 
blood. 

This  theory  has  been  overthrown  by  more  recent  experi- 
menters. 

Another  hypothesis  which  has  attracted  much  attention 
is,  that  the  phenomena  of  uraemia  are  due  to  cerebral  anae- 
mia  and  the  attending  cerebral  oedema. 

Still  more  recent  experimenters  have  claimed  that  urea  is 
formed  in  the  kidneys  from  nitrogenous  material  in  the 
blood,  and  that  ursemic  manifestations  mainly  depend  upon 
the  accumulation  in  the  blood  of  creatin  and  creatinin. 

Again,  others  have  claimed  that  the  phenomena  of  uraemia 
are  due  to  the  retention  in  the  circulation  of  the  products 
of  nerve-waste. 

It  has  also  been  claimed  that  some  forms  of  uraemia  may 
be  associated  with  structural  changes  in  the  brain  similar  to 
those  which  occur  in  the  retina  in  cases  o£  neuro-retinitis. 

The  experiments  and  facts  upon  which  these  theories  are 
based,  lead  me  to  the  following  conclusions  : 

First. — That  unemic  toxaemia  depends  upon  a  complete 
or  partial  arrest  of  the  urinary  secretion. 

Second. — A  qualitative  analysis  of  the  constituents  of 
the  urine  goes  to  show  that  urea  is  its  only  positive  poison- 
ous ingredient,  and  that  it  is  not  the  special  product  of  any 
particular  tissue  or  organ,  but  the  united  product  of  all 
nitrogenized  effete  matter. 

Third. — Numerous  experiments  have  shown  that  urea, 
when  introduced  into  the  blood  of  animals,  acts  as  a  nar- 
cotic poison,  producing  phenomena  identical  with  those  of 
uraemia. 


444  ACUTE   UKJEMIA. 

Fourth. — That  urea  is  not  decomposed  into  carbonate  of 
ammonia  and  water  in  the  blood,  but  that  such  decompo- 
sition may  take  place  outside  the  blood-vessels,  in  the 
bladder,  pelvis  of  the  kidneys,  and  intestines,  and  if  the 
products  of  the  decomposition  are  retained  in  these  cavities 
any  length  of  time,  they  give  rise  to  conditions  of  ammo- 
nsemia,  which  in  many  of  its  features  resembles  ursemia. 

While  the  question  is  still  unsettled  as  to  the  exact  poi- 
sonous agent  in  ursemia,  it  seems  to  me  that  the  facts  rela- 
tive to  urea  warrant  the  assumption  that  urea  is  an  irritant 
poison,  and  when  in  excess  in  the  circulation,  acts  primarily 
upon  the  cerebro- spinal  centres,  and  through  them  inter- 
feres more  or  less  with  the  functions  of  organic  life ;  and 
that  oedema  of  the  brain,  and  other  structural  changes 
which  occur  in  the  course  of  ursemia,  are  the  result  of  the 
action  of  the  poison. 

SYMPTOMS. — An  acute  ursemic  attack  is  usually  preceded 
by  certain  premonitory  signs,  such  as  oedema  in  various 
parts  of  the  body,  restlessness,  or  an  almost  irresistible 
desire  to  sleep,  vertigo,  headache,  delirium,  nausea,  vomit- 
ing, and  impaired  vision.  The  countenance  has  a  pale, 
waxy,  or  dingy  appearance,  and  the  urine  is  scanty,  high- 
colored,  bloody,  albuminous,  and  contains  casts. 

The  progress  of  the  mischief  will  vary  in  different  cases 
according  to  the  amount  and  cause  of  the  retention  of  the 
urea.  If  a  large 'amount  of  urea  is  suddenly  thrown  into 
the  circulation,  and  retained  by  a  continuance  of  the 
arrested  elimination,  or  increased  by  a  continuance  of  the 
producing  cause,  the  body  and  extremities  become  violently 
convulsed,  or  the  patient  passes  rapidly  into  a  state  of 
coma. 

The  convulsions  may  consist  of  a  single  paroxysm,  or  a 
succession  of  paroxysms  may  follow  one  another  at  inter- 
vals of  a  few  minutes  or  several  hours,  the  patient  lying 
during  the  interval  in  a  state  of  more  or  less  profound 
insensibility. 

During  the  convulsion  the  face  becomes  livid,  the  eyes 
are  glassy,  with  the  pupils  contracted  or  dilated.  At  the 
commencement  of  the  convulsive  attack,  they  are  generally 


SYMPTOMS.  445 

contracted,  frothy  mucus,  which  is  sometimes  bloody, 
collects  around  the  mouth,  and  there  is  a  strong,  urinous 
odor  emanating  from  the  perspiration.  The  pulse  is  accel- 
erated, and  the  temperature  is  raised  in  some  instances  as 
high  as  107°  F. 

Urcemic  coma  may  come  on  gradually,  twenty-four  or 
forty-eight  hours  elapsing  before  the  stupor  is  complete,  or 
the  patient  may  fall  suddenly  into  a  state  of  profound 
coma,  its  advent  resembling  an  attack  of  cerebral  apoplexy. 
There  are  periods  when  the  coma  is  so  profound  that  noth- 
ing arouses  the  patient ;  at  other  times  he  is  easily  aroused, 
or  arouses  himself,  and.  attempts  to  speak  and  sit  up, 
swallowing  fluids  with  difficulty. 

When  urea  is  gradually  introduced  into  the  circulation 
or  is  freely  eliminated,  as  in  cases  where  renal  disease  is 
slowly  developed,  the  system  becomes  accustomed  to  the 
presence  of  the  poison,  and  thus  a  considerable  excess  of 
urea  may  exist  in  the  blood  for  a  long  period  without  giving 
rise  to  any  but  the  premonitory  symptoms  of  acute  uraemia. 
When  once  the  balance  is  destroyed  and  a  certain  excess  of 
area  in  the  blood  is  reached,  the  kidneys  become  embar- 
rassed by  the  excessive  demand  made  on  their  excreting 
power,  and  rapid  and  intense  renal  congestion  follows,  the 
nerve-centres  are  overwhelmed,  we  have  either  convulsions 
or  coma,  or  both,  and  thus  acute  uraemia  may  be  developed 
in  the  chronic  as  well  as  the  acute  stage  of  renal  disease. 

Uraemic  coma  is  always  accompanied  by  a  certain  amount 
of  stertor  ;  at  first  the  respirations  are  accelerated,  but  they 
soon  become  slow  and  labored  ;  the  pupils  are  dilated,  but 
the}7  are  not  irregular ;  the  pulse  is  more  rapid  than 
natural,  and  lacks  firmness ;  at  first,  the  temperature  is 
raised,  but  after  a  time  it  falls  below  the  normal  standard. 

Acute  uraemia  simulates  in  some  of  its  phenomena  so 
many  diseases  in  which  convulsions  and  coma  are  the  lead- 
ing symptoms,  that  it  is  difficult  to  give  you  such  directions 
as  will  enable  you  to  make  a  correct  differential  diagnosis 
between  it  and  other  analogous  disorders.  I  will  endeavor 
to  name  a  few  of  the  more  prominent  points  of  difference. 

DIFFEKENTIAL  DIAGNOSIS. — The  phenomena  of  an  epi- 


446  ACUTE   URJEMIA. 

leptic  seizure  are  almost  identical  with  those  of  uraemia, 
and  in  some  instances  the  task  of  distinguishing  the  one 
from  the  other  will  be  very  difficult,  unless  we  admit  the 
previous  history  of  the  patient.  If  this  is  known,  the 
chronic  character  of  the  epilepsy  is  sufficient  to  distinguish 
it  from  acute  uraemia,  and  an  examination  of  the  urine  will 
determine  the  uraemic  character  of  the  convulsions. 

At  the  time  of  the  convulsion  a  distinction  may  also  be 
drawn,  for  in  epilepsy  one  side  is  convulsed  more  violently 
than  the  other ;  while  in  uraemia,  both  sides  of  the  body 
are  equally  affected  by  the  convulsive  movements.  In  epi- 
lepsy, although  there  is  a  loss  of  consciousness,  reflex  sen- 
sibility continues  from  the  beginning  to  the  end  of  the  par- 
oxysm, which  is  not  the  case  in  uraemia.  Immediately  fol- 
lowing uraemic  convulsions  there  is  deep  coma  ;  following 
an  epileptic  seizure  there  is  merely  a  deep  sleep  from  which 
the  patient  may  be  aroused. 

In  cerebral  apoplexy,  coma  always  precedes  convulsions, 
and  with  the  convulsions  there  is  facial  paralysis  and  hemi- 
plegia ;  there  is  also  clonic  spasm  of  the  paratyzed  parts, 
and  the  urinary  symptoms  of  uraemia  are  absent. 

In  hysterical  convulsions,  with  a  scream  the  patient  falls 
into  a  convulsive,  tetanic,  or  cataleptic  condition.  Close 
inspection  shows  that  the  patient  is  not  unconscious,  the 
pupils  are  normal,  as  are  the  pulse  and  temperature.  The 
limbs  are  jerked  irregularly,  the  breathing  is  spasmodic  and 
is  attended  by  a  choking  sensation.  There  is  no  lividity  of 
the  face  nor  distention  of  cervical  blood-vessels,  and  the 
close  of  the  paroxysm  is  usually  accompanied  by  the  dis- 
charge of  a  large  quantity  of  pale  urine. 

Cholcemic  convulsions,  or  those  which  occur  when  the 
blood  is  overcharged  with  the  constituents  of  the  bile,  in 
their  phenomena  very  closely  resemble  uraemia,  but  may  be 
distinguished  from  it  by  the  jaundice  which  precedes  or 
accompanies  their  development,  and  by  the  antecedent 
history  of  acute  hepatic  affections. 

Convulsions  originating  in  meningitis  and  other  cerebral 
affections,  are  distinguished  by  the  accompanying  char- 
acteristic symptoms  of  these  affections. 


DIFFERENTIAL  DIAGNOSIS.  447 

The  main  points  in  the  differential  diagnosis  of  uramic 
coma  are  identical  with  those  of  ursemic  convulsions.  It 
may  be  distinguished  from  the  coma  of  apoplexy  by  the 
absence  of  paralysis.  From  opium  poisoning  it  may  be 
distinguished  by  the  rise  in  temperature.  The  temperature 
in  ursemic  coma  is  generally  above  100°  F.,  while  in  the 
coma  resulting  from  opium  poisoning  it  is  often  below  the 
normal  standard.  In  opium-coma,  the  respiration  is  of  a 
slow  and  peculiar  character,  and  the  pupils  are  uniformly 
contracted.  The  contraction  of  the  pupils  alone  is  not  a 
safe  guide  in  diagnosis,  as  this  frequently  occurs  in  urae- 
mia. 

Ursemic  coma  is  distinguished  from  epileptic  coma  by  the 
antecedent  history  of  the  patient,  and  from  rum-coma  by 
the  alcoholic  surroundings  of  alcoholismus. 

In  all  cases  of  coma,  a  chemical  and  microscopical  exam- 
ination of  the  urine  is  necessary  in  order  to  make  a  per- 
fectly reliable  diagnosis. 

PROGNOSIS. — From  the  many  facts,  with  the  experiments 
and  statements  made  by  competent  observers,  as  well  as 
from  the  clinical  history  of  ursemia,  it  is  evident  that  the 
primary  cause  of  death  in  acute  ursemia  is  a  narcotic 
poison,  the  exact  nature  of  which  we  do  not  understand, 
but  which  resembles  in  its  modus  operandi  other  narcotics, 
of  which  belladonna  and  opium  are  the  best  types. 

The  primary  action  of  this  poison  is  on  the  nerve-centres, 
producing  certain  changes  in  the  blood  which  interfere 
with  or  arrest  oxygenation.  This  action  is  followed  by 
certain  structural  changes  which  take  place  in  the  different 
tissues  of  the  body,  which  make  up  the  post-mortem 
history  of  the  disease. 

When  this  poison  is  introduced  into  the  circulation  in 
small  quantities,  so  that  its  elimination  can  be  effected  in  a 
short  time,  it  only  temporarily  disturbs  the  functions  of 
organic  life ;  but  when  the  nerve-centres  are  overwhelmed 
by  the  introduction  of  large  quantities  of  the  poison,  oxidi- 
sation of  the  blood  is  arrested,  and  it  undergoes  certain 
changes  which  render  it  incapable  of  supporting  life. 

The  prognosis,  then,  in  each  case  of  acute  ursemia,  de- 


448  ACUTE   URJEMIA. 

pends  upon  the  amount  of  urea  in  the  circulation,  and  the 
length  of  time  the  system  has  been  under  its  influence. 

If  the  symptoms  of  excessive  ureemic  toxaemia  are  pres- 
ent, and  there  are  evidences  that  the  poisoning  has  been 
going  on  for  a  considerable  time,  the  prognosis  is  much 
more  unfavorable  than  when  the  acute  ursemic  symptoms 
are  mild  and  of  recent  date. 

TREATMENT. — In  speaking  of  the  treatment  of  this  affec- 
tion, I  shall  first  give  a  brief  synopsis  of  the  most  promi- 
nent views  of  the  present  day,  the  views  of  the  standard 
authorities.  All  agree  in  this,  that  in  the  treatment  of 
acute  uraemia,  to  secure  as  rapidly  as  possible  a  free  elimi- 
native  action,  either  by  the  skin  or  bowels,  or  by  both,  or 
by  the  kidneys,  is  of  first  importance. 

With  most  authorities,  the  favorite  method  of  elimina- 
tion is  diaphoresis,  accomplished  by  vapor  or  hot  air.  It  is 
claimed  that  by  a  vicarious  action  of  the  skin,  the  excre- 
mentitious  products  which  usually  the  kidneys  excrete,  are 
removed  from  the  system  in  the  perspiration. 

In  connection  with  this  process  of  elimination,  a  vicarious 
action  of  the  bowels  is  induced  by  the  internal  administra- 
tion of  drastic  purgatives ;  electarium  and  scammony  are 
most  used  to  accomplish  this  hydragogue  catharsis,  and  it 
is  also  claimed  that  by  this  method  the  alimentary  canal 
eliminates  the  products  which  should  normally  find  their 
way  out  of  the  body  in  the  urine. 

We  have  conflicting  testimony  in  regard  to  the  use  of 
diuretics  in  the  treatment  of  acute  uraemia.  Many  object 
to  their  use  on  the  ground  that  it  is  contrary  to  the  princi- 
ples of  medicine  to  stimulate  an  inflamed  part, — that  the 
first  step  toward  the  healing  of  an  inflamed  organ  is  rest. 
Even  if  we  admit  this  view  to  be  correct,  we  have  a  class  of 
diuretics  that  do  not  act  as  stimulants  to  the  kidneys. 
Digitalis  ranks  first  in  this  list ;  although  it  is  a  very  effi- 
cient diuretic,  it  never  seems  to  irritate  the  kidneys.  It 
increases  the  power  of  the  heart's  action,  and  perhaps  the 
contractile  power  of  the  capillaries ;  it  also  materially  in- 
creases the  blood-pressure.  In  a  healthy  state,  the  normal 
secretion  depends  upon  there  being  no  obstruction  to  that 


TKEATMENT.  449 

pressure.  In  this  disease  the  diminished  flow  of  urine  is  due 
to  obstruction  to  the  capillary  circulation  of  the  kidneys. 
Digitalis,  by  increasing  the  heart-power  and  the  force  of 
the  capillary  circulation,  overcomes  such  obstruction. 

Accepting  this  view  of  the  diuretic  action  of  digitalis,  its 
administration  is  especially  indicated  in  acute  uraemia.  To 
obtain  its  effects  in  the  condition  of  the  kidneys  which 
attends  acute  uraemia,  I  am  convinced  that  much  larger 
doses  are  required  than  are  usually  administered.  My  rule 
of  practice  in  these  cases  is  to  give  half  an  ounce  of  the 
infusion  of  the  English  leaves  every  three  hours  for 
twenty-four  hours,  or  at  least  until  I  produce  the  specific 
effect  of  the  drug,  and  I  do  not  remember  in  a  single 
instance  to  have  met  with  the  overwhelming  accumula- 
tive effects  of  digitalis  against  which  so  many  writers  warn 
us.  Experience,  I  think,  will  sustain  me  in  the  statement, 
that  in  the  majority  of  cases,  when  acute  uraemia  is  fully 
developed,  and  the  patient  is  in  convulsions  or  coma,  the 
skin  and  the  bowels,  as  well  as  the  kidneys,  lose  their  excre- 
tory action,  diaphoresis  cannot  be  induced,  or  if  induced,  it 
is  not  eliminative,  and  the  bowels  do  not  respond  to  purga- 
tives although  the  patient  may  swallow  them  in  large  doses. 
At  one  time,  under  such  circumstances,  free  general  blood- 
letting was  practised  very  extensively  by  the  profession ; 
now  it  has  almost  fallen  into  disuse. 

The  question  then  arises,  if  overwhelming  the  system  by 
the  ursemic  poison  (marked  by  convulsions  and  coma)  shuts 
off  for  a  time  all  the  avenues  of  elimination,  what  means 
have  we  to  counteract  the  effects  of  this  poison,  and  open 
again  the  avenues  of  its  elimination,  or,  at  least,  hold  the 
patient  until  the  normal  eliminating  process  shall  be  re- 
established ?  The  first  thing  to  be  accomplished  is  to  dimin- 
ish reflex  sensibility,  and  subdue  spasmodic  muscular 
paroxysms,  for  these,  if  continued,  either  will  directly  ter- 
minate life,  or  end  in  equally  fatal  insensibility.  The  remedy 
which  for  some  years  has  been  employed  for  the  accomplish- 
ment of  these  results  is  chloroform.  It  has  been  extensively 
used,  and,  I  believe,  is  regarded  the  safest  and  most  reliable 

means  for  controlling  ursemic  convulsions. 
29 


450  ACUTE 

Although  man}r  authorities  recommend  the  use  of  chloro- 
form in  uraemic  eclampsia,  few  make  mention  of  its  employ- 
ment in  acute  uraemia  independent  of  the  puerperal  state. 
Its  only  known  clinical  effect  is  to  control  muscular  spasm, 
and  in  a  large  proportion  of  cases  it  fails  to  give  more  than 
temporary  relief  to  those  patients  who  pass  from  successive 
convulsions  into  a  state  of  complete  coma,  and  die  without 
any  apparent  neutralizing  effect  from  the  chloroform. 

In  the  few  cases  in  which  I  have  administered  chloroform 
in  non-puerperal  ursemic  convulsions,  it  has  seemed  to  me 
to  have  no  other  effect  than  to  arrest  convulsive  movements 
by  rapidly  hastening  my  patient  into  a  state  of  insensibility. 
In  no  instance  have  I  known  its  administration  to  be  imme- 
diately followed  by  diaphoresis,  or  a  return  of  the  urinary 
secretion.  It  has  seemed  to  be  more  difficult  to  establish 
diaphoresis  or  diuresis  by  diaphoretics  and  diuretics  in 
patients  with  uraemia  to  whom  chloroform  had  been  admin- 
istered, than  in  those  who  had  not  taken  it.  Therefore,  I 
believe  that  while  chloroform  temporarily  controls  muscular 
spasm,  it  prejudices  the  chances  of  ultimate  recovery,  by 
the  changes  its  inhalation  produces  in  the  blood,  which 
changes  increase  rather  than  retard  the  development  of  the 
iiraemic  toxaemia.  With  these  impressions  one  naturally 
seeks  an  agent  which  not  only  has  the  power  to  control 
muscular  spasm,  but  at  the  same  time  by  its  action  shall 
tend  to  reopen  the  avenues  of  elimination,  either  by  counter- 
acting the  effects  of  the  uraemic  poison  on  the  nerve-centres, 
and  thus  facilitate  the  action  of  diuretics  and  diaphoretics, 
or  itself  act  directly  as  an  eliminator. 

I  believe  morphine  administered  hypodermically  to  be 
such  an  agent. 

There  are  two  questions  that  very  naturally  present 
themselves  in  connection  with  the  use  of  morphine  in  acute 
uraemia. 

First. — Can  morphine  in  full  doses  be  administered  with- 
out danger  to  patients  with  acute  uraemia  ? 

Second. — What  are  the  effects  of  such  administration  ? 

If  you  turn  to  recognized  authorities  for  an  answer  to 
the  first  of  these  inquiries,  you  will  find  that  nearly  all 


TREATMENT.  451 

make  mention  of  the  use  of  opium  in  ursemic  toxaemia  only 
to  warn  you  against  the  danger  attending  its  administra- 
tion. 

During  the  first  years  of  my  professional  life,  I  regarded 
opium  as  one  of  the  most  dangerous  remedial  agents  that 
could  be  administered  to  ursemic  patients,  rarely  daring  to 
give  more  than  five  grains  of  Dover's  powder  to  a  patient 
with  albuminous  urine,  and  if  fatal  coma  followed  such  ad- 
ministration, more  than  once  do  I  remember  to  have  felt 
that  a  Dover's  powder  which  I  had  administered  might  have 
been  the  cause  of  the  fatal  coma. 

In  1868,  I  administered  my  first  hypodermic  injection  of 
morphine  to  a  patient  with  acute  uraemia. 

The  effects  which  followed  its  administration  in  this  case 
taught  me,  that  in  some  cases  with  marked  ursemic  symp- 
toms, morphine  could  be  administered  hypodermically,  not 
only  with  safety,  but  with  apparent  advantage. 

Since  that  time  I  have  used  hypodermic  injections  of 
morphine  in  the  treatment  of  patients  with  Bright' s  dis- 
ease, especially  when  the  premonitory  symptoms  01  acute 
ursemia  were  present,  as  well  as  during  the  active  mani- 
festations of  ursemic  intoxication,  and  so  far  as  1  am  able 
to  judge,  its  administration  has  been  uniformly  followed 
by  good  results.  In  no  instance  am  I  aware  that  I  have 
caused  a  fatal  narcotism. 

From  the  histories  of  quite  a  large  number  of  puerperal 
and  non-puerperal  cases  of  acute  ursemia,  in  which  mor- 
phine was  successfully  used  (some  of  which  I  have  reported 
in  the  medical  journals),  I  have  reached  the  following  con- 
clusions : 

First. — That  morphine  can  be  administered  hypoder- 
mically to  some  if  not  to  all  patients  with  acute  ursemia, 
without  endangering  life. 

Second. — That  the  almost  uniform  effect  of  morphine  so 
administered  is,  first,  to  arrest  muscular  spasms  by  counter- 
acting the  effect  of  the  ursemic  poison  on  the  nerve-centres  ; 
second,  to  establish  profuse  diaphoresis  ;  third,  to  facilitate 
the  action  of  cathartics  and  diuretics,  especially  the  diuretic 
action  of  digitalis. 

.  i-rr    Olr    I  M 

COLLLbb  L  Q 


452  ACUTE  URAEMIA. 

Thus  morphine  administered  hypodermically,  becomes  a 
powerful  eliminating  agent. 

The  rules  which  are  to  govern  its  administration  are  as 
yet  not  well  defined.  My  own  experience  would  teach  me 
to  give  small  doses  at  first,  not  to  exceed  ten  minims.  If 
convulsions  threaten?  and  a  small  dose  does  not  arrest  the 
muscular  spasms,  it  may  be  increased  to  twenty  minims, 
and  the  hypodermics  may  be  repeated  as  often  as  every 
two  hours.  It  must  be  given  in  sufficient  quantities  to 
control  convulsions  ;  neither  the  contraction  of  the  pupils 
nor  the  number  of  the  respirations  is  a  reliable  guide  in  its 
administration. 

I  would  not  discard  all  (perhaps  none)  of  those  means 
which  have  been  relied  on  for  the  relief  of  patients  in  acute 
uraemia,  but  would  call  your  attention  to  the  fact,  that  in  a 
certain  proportion  of  cases  (if  not  in  all)  of  acute  uraemia, 
hypodermic  injections  of  morphine  will  not  only  control 
muscular  spasms,  but  aid  in  establishing  the  eliminating 
processes,  and  thus  become  another  means  of  saving  life  in 
these  too  often  fatal  cases. 


*  f'  /  f  <'  I  fc  ','  P  rr 

,  r.   -  ff     =  •=  ,   - 


LECTURE    XXXVIII. 


BRIGHT' S  DISEASES  OF  THE  KIDNEY. 


Definition  of  the  Term.— Parenchymatous  Nephritis,  (Morbid  Anatomy) • 

Amyloid  Degeneration  of  the  Kidneys,  (Morbid  Anatomy). 


THIS  morning  I  shall  commence  the  history  of  a  very 
important,  and  at  the  same  time,  a  very  common  group  of 
diseases,  which  are  now  classed  under  the  comprehensive 
term  of  Bright*  s  diseases  of  the  kidneys. 

Dr.  Bright,  whose  name  this  class  of  diseases  bears,  first 
called  the  attention  of  the  profession  to  them  in  the  year 
1827,  at  which  time  he  described  and  represented  by  colored 
drawings,  various  morbid  appearances  of  the  kidneys  which 
he  showed  were  of  every-day  occurrence,  and  that  they 
were  very  frequently  associated  with  general  dropsy.  He 
was  the  first  systematic  investigator  in  the  great  field  of 
renal  pathology. 

Dr.  Bright  regarded  granular  degeneration  as  the  prin- 
cipal if  not  the  only  pathological  lesion  present  in  this  class 
of  diseases  ;  he  accordingly  designated  it  as  a  granular 
nephritis.  More  recent  and  more  extended  investigations 
have,  however,  shown  that  there  are  several  morbid  pro- 
cesses in  the  kidneys  of  those  who  are  the  subjects  of  this 
form  of  disease  ;  it  has  also  been  shown  that  the  kidneys  in 
the  course  of  these  morbid  processes  present  a  great  variety  of 
appearances,  and  you  will  find  in  your  text-books  a  great 
variety  of  terms  claiming  to  be  expressive  of  these  different 
morbid  appearances.  You  will  find  mentioned  the  large 
white  kidney,  the  large  granular  kidney,  the  small  granular 


454  BRIGHT' s  DISEASE  OF  THE  KIDXEYS. 

kidney,  the  large  and  small  red  granular  kidney,  the  waxy 
kidney,  and  the  cirrhotic  kidney ;  all  of  these  different  vari- 
ties  are  described  by  different  writers  under  the  head  of 
Bright' s  diseases  of  the  kidneys. 

Almost  necessarily  you  become  confused  when  you  at- 
tempt to  harmonize  the  description  of  the  morbid  anatomy 
of  this  class  of  diseases,  as  given  by  different  medical  au- 
thorities. 

I  shall  not  attempt  to  compare  and  analyze  the  various 
descriptions  of  the  anatomical  changes  which  occur  in 
Bright' s  diseases,  as  given  by  medical  writers,  but  adopt 
the  one  which  seems  to  me  to  include  all  descriptions 
and  at  the  same  time  renders  intelligible  these  different 
anatomical  processes. 

Before  proceeding  to  the  description  of  the  morbid  changes 
which  occur  in  this  group  of  diseases,  let  me  impress  upon 
your  minds  that  there  are  three  distinct  anatomical  elements 
in  the  kidney  which  are  primarily  or  secondarily  involved 
in  these  morbid  changes  ;  namely,  the  uriniferous  tubules, 
the  blood-vessels,  and  the  intertubular  tissue. 

Now,  in  the  different  forms  of  kidney  changes  included 
under  the  head  of  Bright' s  diseases,  the  morbid  processes 
begin  primarily  in  one  of  these  three  elements,  and  it  is 
possible  to  divide  this  group  of  diseases  into  classes  accord- 
ing to  the  anatomical  element  primarily  affected.  For  in- 
stance, you  have  one  form  in  Avhich  the  primary  anatomical 
changes  commence  in  the  uriniferous  tubules.  Again,  you 
have  another  form  in  which  the  primary  changes  commence 
in  the  walls  of  the  vessels.  Then,  you  have  still  another 
form  in  which  the  primary  changes  commence  in  the  inter- 
tubular  tissue. 

All  these  forms  of  morbid  change  may  be  present  in  the 
same  kidney  ;  but  by  a  careful  examination,  you  will  be 
able  to  determine  in  which  class  of  anatomical  elements  the 
primary  morbid  processes  commenced. 

I  shall  for  the  most  part  adopt  the  arrangement  of 
Virchow,  as  modified  by  Dr.  Stewart,  and  describe  this 
group  of  diseases  iinder  three  distinct  heads  : 

First. — A   form   in  which   the   anatomical   changes   are 


MOKBID   ANATOMY.  455 

inflammatory  in  their  nature,  and  commence  in  the  urinif- 
erous  tubules.  This  form  has  been  designated  parenchy- 
matous nephritis,  or  the  inflammatory  form  of  Bright' s 
disease. 

Second. — A  form  which  is  non-inflammatory,  in  which 
the  anatomical  changes  commence  in  the  walls  of  the  blood- 
vessels. This  has  been  designated  the  amyloid  form  of 
Bright' s  disease. 

Third. — A  form  in  which  the  anatomical  changes  com- 
mence in  the  intertubular  tissue.  This  form  has  been 
designated  the  cirrhotic form  of  Bright' s  disease. 

Under  these  three  heads  I  shall  endeavor  to  describe  all 
the  different  changes  which  are  met  with  in  the  kidneys  of 
those  who  die  having  had  the  prominent  symptoms  of 
Bright' s  disease,  namely,  albumen  and  casts  in  the  urine, 
with  dropsy. 

The  order  which  I  shall  observe  in  the  study  of  these 
three  forms  of  disease  will  be — first,  to  consider  the  morbid 
anatomy  of  each  in  succession,  after  which  I  shall  separ- 
ately consider  the  remaining  portion  of  the  history  of  each 
form. 

PAHENCHYMATOU3  NEPHRITIS  (Morbid,  Anatomy). 

This  is  the  inflammatory  form  of  Bright' s  disease,  and  by 
far  the  most  common  form  of  the  disease.  It  may  pursue 
an  acute  or  chronic  course,  be  of  short  or  long  duration, 
and  vary  both  in  the  character  and  intensity  of  the  inflam- 
matory processes. 

If  it  passes  through  its  entire  course,  it  may  be  divided 
into  three  stages  :  first,  a  stage  of  inflammation ;  second, 
a  stage  of  degeneration,  either  fatty  or  granular ;  third,  a 
stage  of  atrophy. 

The  first  stage  of  parenchymatous  nephritis  corresponds 
to  that  form  of  Bright' s  disease  usually  denominated  acute 
albuminuria,  or  acute  desquamative  or  tubular  nephritis. 
I  prefer  acute  parenchymatous  nephritis  to  any  of  these 
terms. 

MORBID  ANATOMY. — In  the  first,  or  inflammatory  stage  of 
parenchymatous  nephritis,  the  gross  and  microscopical  ap- 


456  PAEENCIIYMATOITS   NEPHRITIS. 

pearance  of  the  kidneys  will  vary  according  to  the  character 
of  the  inflammatory  process,  which  may  be  either  catarrhal, 
croupous,  or  desquamative.  All  of  these  varieties  of  inflam- 
matory processes  are  embraced  under  the  general  head  of 
the  first  stage  of  parenchymatous  nephritis. 

The  kidneys  are  usually  increased  in  size,  their  capsules 
non-adherent,  their  surface  smooth  and  mottled,  presenting 
an  irregular  combination  of  red  vascular  engorgement  and 
unnatural  pallor  ;  sometimes  they  are  of  a  dark  and  purplish 
color,  dotted  here  and  there  with  spots  of  ecchymosis.  On 
section,  the  cortical  portion  is  relatively  increased  in  volume 
and  is  dotted  over  its  entire  cut  surface  with  dark  or  bright 
red  points,  which  correspond  to  the  situation  of  the  Mal- 
pighian  tufts,  which,  in  some  instances,  stand  out  promi- 
nently upon  its  surface.  The  cortical  substance  between  the 
Mapighian  tufts  may  be  of  a  paler  color  than  natural.  The 
engorgement  will  usually  be  most  marked  at  the  base  of  the 
pyramids,  at  the  junction  of  the  cortical  and  medullary 
substance  ;  it  is  even  more  intense  at  that  point  than  at  the 
Malpighian  tufts.  The  medullary  portion  will  be  of  a  darker 
color  than  normal,  darker  even  than  the  cortical  portion  ; 
sometimes  it  will  present  a  streaked  appearance  (red  and 
white  lines  alternating)  ;  the  lighter  lines  correspond  to  the 
changed  uriniferous  tubes.  The  lining  membrane  of  the 
pelvis  of  the  kidney  is  usually  somewhat  congested. 

When  such  a  kidney  is  examined  microscopically,  it  may 
be  found  to  present  quite  a  variety  of  appearances,  varying 
with  the  character  of  the  inflammatory  processes.  First, 
you  may  find  the  uriniferous  tubules  the  seat  of  a  simple 
catarrhal  process ;  then,  the  epithelial  lining  may  become  par- 
tially or  completely  lifted  from  its  normal  situation,  disappear 
and  the  tubules  become  more  or  less  filled  with  cells  which 
correspond  to  those  new  cell-formations  which  have  been 
described  as  present  in  catarrhal  inflammations  affecting 
other  mucous  surfaces.  There  will  also  be  more  or  less  cell 
infiltration  around  the  tubules  in  the  intertubular  tissue. 

This  catarrh  of  the  uriniferous  tubes  is  of  frequent  occur- 
rence,  but  usually  passes  unrecognized,  as  it  gives  rise  to 
very  few  objective  symptoms.  Again,  in  another  class  of 


MORBID  ANATOMY.  457 

cases,  you  will  find  that  the  centre  of  the  uriniferous  tubes 
contains  a  hyaline  material  which  unquestionably  is  coagu- 
lated fibrin  ;  this  hyaline  material  may  have  mingled  with  it, 
or  may  be  surrounded  by  epithelium  and  blood-globules  ;  it 
undoubtedly  is  an  inflammatory  exudation,  and  resembles 
the  products  of  croupous  inflammation. 

Again,  in  another  class  of  cases,  all  the  inflammatory 
changes  commence  in  the  epithelial  cells  of  the  uriniferous 
tubes ;  these  become  cloudy,  their  nuclei  disappear,  and 
they  become  distended  and  granular,  desquamation  follows, 
and  the  tubes  become  filled  with  broken-down  epithelium 
and  fatty  matter ;  this  process  has  been  termed  by  some, 
chronic  desquamative  nephritis,  but  at  its  commencement  it 
has  all  the  characteristics  of  an  active  inflammatory  process. 

In  the  first  stage  of  the  inflammatory  form  of  Bright' s 
disease,  you  may  have  any  one  of  these  three  processes  es- 
tablished, or  you  may  have  them  all  present  at  the  same  time 
in  the  same  kidney  ;  but  they  all  have  their  primary  seat 
in  the  uriniferous  tubules.  While  these  tubular  changes 
are  being  developed,  new  cell-formative  changes  may  take 
place  in  the  intertubular  tissue.  Then,  in  the  first  stage 
of  parenchymatous  nephritis  we  may  have  the  following 
changes  ;  first,  more  or  less  intense  congestion  attended  by 
very  active  proliferation  and  desquamation  of  the  epithelial 
lining  of  the  uriniferous  tubules  ;  the  material  thus  thrown 
out  blocks  up  and  distends  these  tubes.  Second,  the  con- 
gestion may  produce  rupture  of  the  capillary  vessels,  and 
blood-globules  may  escape  into  the  tubes  with  the  epithe- 
lium. Then  again,  the  interrupted  circulation  may  cause 
an  effusion  of  fibrin,  which  coagulates  in  the  tubes  and 
mingles  with  the  epithelial  cells  and  blood-globules.  In 
cases  which  result  from  scarlatina,  the  catarrhal  and  exuda- 
tive process  is  united  to  the  desquamative.  In  the  latter 
part  of  this  stage,  the  contents  of  the  tubules  become 
changed  into  an  amorphous  mass.  If  the  inflammatory 
stimulus  is  continued,  fatty  changes  follow. 

In  a  certain  proportion  of  cases  of  this  form  of  Bright' s 
disease,  the  inflammatory  processes  run  an  acute'  course, 
and  quickly  terminate  either  in  recovery  or  death  ;  a  cer- 


458  PAKEXCIIYMATOUS   NEPHRITIS. 

tain  proportion,  however,  become  chronic,  and  the  changes 
which  the  kidneys  undergo  vary  according  to  the  form 
of  the  degenerative  inflammatory  changes  which  may  be 
established. 

This  brings  us  to  the  second  or  degenerative  stage  of  par - 
encliymatous  nephritis,  or,  as  it  is  sometimes  called,  the 
fatty  stage  of  the  inflammatory  form  of  Bright' s  disease. 

In  this  stage  the  active  inflammatory  processes  have 
ceased,  and  the  degenerative  processes  have  commenced,  or 
if  epithelial  degeneration  has  been  the  primary  lesion,  fatty 
transformation  commences. 

It  is  a  legitimate  consequence  of  depraved  cell-growth, 
and  may  make  -its  appearance  in  any  form  of  renal  lesion 
in  which  there  is  a  protracted  interference  with  the  normal 
condition  of  the  uriniferous  tubes  ;  at  first,  but  few  of  the 
epithelial  cells  of  the  uriniferous  tubes  undergo  the  fatty 
change,  but  as  the  transformation  becomes  general,  the 
entire  contents  of  the  tubules  become  loaded  with  minute 
oil-globules,  and  this  constitutes  the  stage  of  fatty  degen- 
eration. The  kidneys  are  now  enlarged,  their  capsules  are 
non-adherent,  surface  is  smooth ;  color  is  paler  than  na- 
tural, presenting  a  more  or  less  yellow  appearance  ;  some- 
times it  is  mottled ;  stellate  or  punctate  congestion  is 
usually  more  or  less  marked.  On  section,  you  will  find  that 
the  enlargement  of  the  organ  is  due  chiefly  to  an  increase 
in  the  volume  of  the  cortical  substance,  which  is  of  a  pale 
yellowish-white  color  ;  there  is  but  little  change  in  the  me- 
dullary portion.  The  Malpighian  tufts  do  not  stand  out 
prominently  as  in  the  first  stage,  for  there  is  more  or  less 
fatty  material  in  the  dilated  portion  of  the  uriniferous  tubes 
around  the  Malpighian  tufts,  which  gives  them  somewhat 
of  a  pale  appearance.  The  vascularity  of  the  whole  kidney 
seems  to  be  very  much  diminished.  As  in  the  first  stage, 
the  principal  changes  take  place  in  the  convoluted  tubes  of 
the  cortical  portion,  and  in  that  portion  of  the  tubules 
which  surrounds  the  Malpighian  tufts.  Thin  sections  of 
the  cortical  substance  of  a  kidney  in  this  stage  of  degenera- 
tion are  very  opaque  and  show  little  more  by  the  microscope 
than  uriniferous  tubules  distended  with  fatty  granules  ;  the 


MORBID   ANATOMY.  459 

tubules  are,  however,  irregularly  distended  with  this  ma- 
terial. At  some  points  they  are  greatly  increased  in  size,  at 
other  points  they  are  of  normal  calibre.  In  the  Malpighian 
tufts  are  found  oil-globules  more  or  less  abundantly,  but 
the  capillaries  of  the  tuft  are  unchanged. 

It  is  possible  for  recovery  to  take  place  after  a  kidney 
has  reached  the  stage  of  fatty  transformation  ;  the  degener- 
ative process  may  be  arrested  by  the  re-establishment  of  the 
normal  circulation  in  the  kidneys,  the  fatty  material  may 
be  removed  from  the  tubules,  and  the  epithelial  lining  of 
the  tubes  be  restored. 

If  the  interference  with  the  circulation  and  nutrition  of 
the  kidneys  is  continued,  atrophy  or  granular  degeneration 
of  the  organs  necessarily  follows.  Some  claim  that  renal 
atrophy  and  granular  degeneration  of  the  kidneys  are  the 
same  ;  that  the  granular  degeneration  is  a  form  of  atrophy. 
One  thing  seems  to  me  very  certain,  that  both  of  these  pro- 
cesses are  associated  with  or  the  result  of  long-continued 
active  or  passive  renal  congestion,  which  has  already 
induced  in  the  kidneys  some  one  of  the  changes  which  have 
been  described.  These  prior  tubular  changes  may  or  may 
not  have  been  ushered  in  and  attended  by  acute  symptoms. 

After  the  fatty  transformation  has  been  established  under 
the  continued  morbid  stimulus,  cellular  elements  are  devel- 
oped in  the  walls  of  the  tubes  and  in  the  intertubular 
tissue,  which  pass  through  the  changes  of  new  tissue  forma- 
tions ;  contraction  of  the  new  material  follows,  thickening 
of  the  blood-vessels  and  tubules  is  gradually  developed,  and 
the  processes  of  inflammatory  atrophy  are  slowly  pro- 
gressing. At  the  same  time,  the  contents  of  the  tubules 
and  the  epithelium  are  constantly  undergoing  fatty  and 
granular  degeneration. 

The  contractions  which  occur  in  the  new  tissue-formations 
may  constrict  the  uriniferous  tubules  at  various  points,  and 
thus  cause  the  development  of  cysts,  varying  in  size  from  a 
pin's  head  to  that  of  a  pea  or  even  larger.  In  this  form 
of  kidney  degeneration,  there  is  never  that  amount  of  new 
tissue  increase  which  occurs  in  the  gouty  or  cirrhotic  kidney. 
You  will  necessarily  find  that  kidneys  which  have  passed 


460  PARENCHYMATOUS   NEPHRITIS. 

into  the  atrophied  stage  of  parenchymatous  nephritis, 
present  a  variety  of  appearances,  and  are  always  more  or 
less  diminished  in  size.  Their  surface  is  uneven  and  more 
or  less  nodular,  their  capsules  are  adherent,  and  when  re- 
moved, portions  of  kidney-tissue  are  removed  with  them, 
leaving  the  denuded  surface  of  the  organs  uneven  and  pre- 
senting an  appearance  more  or  less  granular,  often  bearing 
a  striking  resemblance  to  a  sluggish  granulating  ulcer.  The 
color  varies,  it  may  be  white  with  a  few  stellate  vessels  here 
and  there  on  its  surface,  or  it  may  present  an  unnaturally 
red  or  mottled  appearance. 

On  section,  it  will  be  found  that  the  diminution  in  the 
size  of  the  kidneys  is  mainly  due  to  atrophy  of  the  cortical 
substance ;  the  medullary  portion  retains  very  nearly  its 
normal  dimensions ;  the  loss  of  the  cortical  substance  may  be 
so  complete  that  the  medullary  portion  of  the  organ  appears 
to  extend  almost  to  its  surface ;  the  cortical  substance 
between  the  pyramids  will  also  be  more  or  less  atrophied. 
The  whole  is  firm  and  tough,  not  easily  broken  down  under 
pressure ;  the  capsule  is  not  only  adherent,  but  slightly 
thickened. 

On  making  a  microscopical  examination  of  sections  of 
the  cortical  substance  of  a  kidney  in  this  stage  of  nephritis, 
a  noticeable  feature  will  be  the  great  hypertrophy  of  the 
stroma  of  the  organ  at  the  expense  of  vessels  and  tubules. 
You  will  find  the  walls  of  the  vessels  thickened  either  by 
formative  inflammatory  changes  which  have  taken  place  in 
the  walls  themselves,  or  an  increase  in  the  tissues  which 
surround  them.  The  Malpighian  tufts  will  have  lost  their 
distinctness  on  account  of  the  thickening  of  their  capsules, 
and  the  reduced  size  of  the  capillaries  of  the  tufts. 

The  uriniferous  tubules  will  be  found  filled  in  some  places 
with  granular  or  fatty  material ;  in  other  places  they  will 
be  entirely  obliterated ;  again,  atrophied  and  more  or  less 
shrivelled.  The  chief  changes  therefore  are,  thickening  of 
the  walls  of  the  blood-vessels,  a  greater  or  less  obliteration 
of  the  uriniferous  tubules,  a  more  or  less  marked  disap- 
pearance of  the  epithelial  lining  from  the  tubules  which  are 
not  obliterated,  as  well  as  evidences  of  fatty  and  granular 


MOEBID  ANATOMY.  461 

degeneration.  There  is  also  a  very  marked  increase  in  the 
walls  of  the  tubules  and  the  capsules  of  the  Malphigian 
tufts.  All  of  these  changes  are  principally  confined  to  the 
cortical  substance. 

The  close  similarity  in  the  appearance  of  a  kidney  in  this 
stage  of  parenchymatous  nephritis  and  a  cirrhotic  kidney, 
has  led  some  observers  to  the  opinion  that  the  degenerative 
processes  are  the  same  in  both  instances.  I  shall  point  out 
their  differences  when  I  come  to  describe  the  anatomical 
changes  of  the  cirrhotic  kidney. 

The  duration  and  termination  of  the  inflammatory  pro- 
cesses in  this  form  of  Bright' s  disease  are  uncertain.  Death 
may  take  place  in  any  stage.  Complete  recovery  from  the 
first  stage  is  not  of  unfrequent  occurrence ;  it  is  possible 
after  the  second  stage  is  reached,  it  is  impossible  after  the 
changes  described  as  occurring  in  the  third  stage  have  taken 
place.  If  all  the  kidney-tissue  is  involved,  recovery  is  almost 
impossible.  You  must  remember  that  in  the  large  propor- 
tion of  instances  of  this  form  of  Bright' s  disease,  the  entire 
kidney-tissue  is  not  involved.  This  is  specially  true  in  those 
cases  in  which  the  primary  changes  consist  in  cloudiness  of 
the  epithelium.  The  inflammatory  process  may  pass  through 
all  its  stages,  and  the  affected  kidney-tissue  become  atro- 
phied, and  yet  there  will  be  enough  of  healthy  kidney-tissue 
remaining  to  properly  perform  the  kidney  function.  This 
fact  has  an  important  bearing  on  the  question  of  prognosis. 

Before  entering  farther  into  the  history  of  parenchyma- 
tous nephritis,  I  will  briefly  consider  the  anatomical  changes 
which  occur  in  the  amyloid  and  cirrhotic  form  of  Bright' s 
disease. 

AMYLOID  FORM  OF  BRIGHT'S  DISEASE. 

We  are  now  to  consider  the  anatomical  changes  which 
occur  in  that  form  of  Bright' s  disease  in  which  the  primary 
changes  take  place  in  the  walls  of  the  blood-vessels.  Amy- 
loid degeneration  is  always  chronic  in  its  course ;  it  has  no 
acute  stage,  and  usually  invades  several  organs  of  the  body 
simultaneously. 


462  AMYLOID.  KIDJSTEr. 

MORBID  ANATOMY. — In  tracing  the  changes  which  occur 
in  the  kidneys,  or  in  any  other  glandular  organ  that  is  the 
seat  of  amyloid  degeneration,  we  find  that  the  walls  of  the 
minute  arteries  are  primarily  affected  ;  then  there  is  added 
changes  in  the  secreting  tubes  or  cells ;  lastly,  the  organ 
undergoes  atrophy. 

For  the  sake  of  convenience  in  description,  the  anatomical 
changes  which  take  place  in  kidneys  which  are  the  seat  of 
amyloid  degeneration,  may  be  divided  into  three  stages. 

First,  a  stage  of  degeneration  of  the  walls  of  the  vessels  ; 
second,  that  in  which  is  added  to  the  changes  in  the  blood- 
vessels, changes  in  the  uriniferous  tubules  ;  third,  a  stage 
of  atrophy. 

In  the  first  stage  there  is  little  change  in  the  general 
appearance  of  the  kidneys.  They  may  be  slightly  increased 
in  size,  firmer  than  normal,  and  allow  their  capsules  to  be 
readily  removed ;  their  surface  is  smooth ;  there  is  no 
marked  evidences  of  congestion ;  sometimes  they  are  of  a 
paler  color  than  normal.  Upon  section,  the  cortical  sub- 
stance presents  either  a  normal  appearance,  or  perhaps  the 
Malpighian  tufts  may  appear  a  trifle  more  prominent  than 
natural,  and  present  the  appearance  of  gray  translucent 
points,  which  reflect  light  better  than  the  surrounding 
tissue. 

A  farther  examination  is  usually  necessary  to  detect  the 
changes  which  have  occurred,  and  that  farther  examination 
consists  in  the  application  of  the  "iodine  test."  When 
properly  used,  you  have  in  iodine  an  infallible  and  easily 
applied  test  for  the  presence  of  amyloid  change,  however 
slight.  Lugol'  s  solution,  diluted  with  water  until  it  is  of  a 
dark  sherry- color,  is  a  very  convenient  form  for  general 
use.  It  may  be  applied  with  a  clean  camel' s-hair  brush 
over  the  suspected  tissue ;  after  a  few  seconds,  if  amyloid 
material  is  present,  the  affected  parts  rapidly  absorb  the 
iodine,  and  assume  a  dark-brown  tint,  easily  distinguishable 
from  the  yellow  stain  upon  the  tissues  not  thus  diseased. 
Upon  microscopic  examination,  assisted  by  iodine,  you  will 
find  in  the  first  stage  of  amyloid  degeneration  of  the  kid- 
neys, that  the  change  in  the  vessels  is  most  marked  in  the 


MOEBID  ANATOMY.  463 

Malpighian  tufts.  It  will  also  be  found  that  the  middle 
coats  of  the  small  arteries  have  undergone  more  or  less 
amyloid  change.  At  first,  these  are  the  only  changes  that 
are  present. 

In  the  second  stage  the  kidneys  will  be  increased  in  size 
—in  some  cases  very  much  increased ;  their  capsules  will 
be  more  adherent,  their  surfaces  will  be  smooth  and  of  a 
pale  color,  with  stellate  vascularity.  On  section,  the  evi- 
dence is  unmistakable  that  the  increase  in  the  size  of  the 
organ  is  due  to  an  increase  of  the  cortical  substance.  The 
medullary  substance  is  not  increased  to  any  extent,  but  the 
blood-vessels  of  that  portion  of  the  kidney  may  undergo  a 
waxy  change,  similar  to  that  which  takes  place  in  the  blood- 
vessels of  the  cortical  substance.  The  normal  anatomical 
outline  of  the  cortical  and  medullary  portion  is  entirely 
lost,  the  Malpighian  tufts  are  indistinct,  and  the  whole 
cortical  substance  has  a  peculiar  waxy  appearance.  When 
a  microscopical  examination  is  made,  the  entire  section  will 
present  a  shining,  yellow  appearance,  as  though  all  the 
tissues  of  the  organ  were  infiltrated  with  the  amyloid  ma- 
terial. The  uriniferous  tubules  are  distended,  particularly 
noticeable  in  the  medullary  portion,  with  a  material  ap- 
parently of  the  same  nature  as  that  which  is  deposited  in 
the  walls  of  the  blood-vessels,  but  the  material  in  the  tubules 
does  not  give  the  amyloid  reaction  by  the  application  of  the 
iodine  test. 

The  material  deposited  in  the  tubes  varies.  It  may  be 
made  up  of  broken-down  epithelium  and  fatty  granules,  or 
a  material,  which  is  fibrinous  in  its  nature,  may  be  pressed 
from  the  tubes  in  the  form  of  large  hyaline  casts  ;  this  ma- 
terial will  not,  however,  give  the  characteristic  reaction  of 
amyloid  material  upon  the  application  of  iodine. 

The  basement  membrane  of  the  tubes  in  the  cortical  and 
tubular  portion  of  the  kidney  is  thickened,  and  sometimes 
the  tubular  portion  is  indistinct  on  account  of  intertubular 
effusion.  The  Malpighian  capillaries  are  thickened,  opaque, 
and  glistening.  All  the  blood-vessels  of  the  kidney  are 
more  or  less  affected  by  the  degeneration,  but  it  is  especially 
apparent  in  the  blood-vessels  which  surround  the  tubules. 


464  AMYLOID   KIDNEY. 

The  cylinders  or  casts  which  in  waxy  kidney  are  formed 
in  the  uriniferous  tubes,  are  usually  situated  in  the  large 
tubes  of  the  pyramids,  and  are  least  abundant  in  the  convo- 
luted tubes ;  fragments  of  cast  material  may  be  seen  not 
unfrequently  extending  as  high  up  as  the  straight  tubes 
extend. 

Amyloid  degeneration  is  of  very  slow  development,  and 
much  time  may  elapse  before  it  will  be  sufficiently  extensive 
to  interfere  materially  with  the  function  of  the  organ. 

In  the  third  stage,  or  stage  of  atrophy,  the  organ  is  very 
much  diminished  in  size.  The  capsule  is  adherent,  the  sur- 
face uneven,  and  of  a  pale,  waxy  appearance. 

Upon  section,  it  will  be  seen  that  the  diminution  in  size  is 
due  to  decrease  of  both  medullary  and  cortical  portion. 
The  Malpighian  tufts  are  large  and  prominent ;  the  small 
arteries  are  enlarged,  and  at  points  are  rendered  impervious 
by  changes  in  their  walls,  producing  a  mechanical  obstruc- 
tion to  the  circulation. 

On  microscopical  examination  of  sections  from  different 
portions  of  the  kidney,  at  all  points  the  tubules  will  be 
found  more  or  less  atrophied  and  their  walls  collapsed. 
The  material  which  was  present  in  them  in  the  second  stage, 
to  a  very  great  extent,  has  disappeared  ;  the  blood-vessels 
generally  will  appear  thickened,  and  their  outline  will  be 
more  or  less  irregular. 

If  there  is  any  doubt  as  to  the  form  of  degeneration  which 
has  brought  about  this  change,  the  brownish-red  color  pro- 
duced by  the  application  of  iodine  upon  the  degenerated 
Malpighian  tufts  will  of  itself  settle  the  question.  The 
degree  of  atrophy  may  vary,  but  however  extensive  it  may 
be,  by  dipping  a  section  in  the  iodine  solution,  and  micro- 
scopically examining  it  with  a  low  power,  you  can  always 
find  abundant  evidence  if  there  is  amyloid  material  in  the 
degenerated  vessels  and  tubes. 

As  regards  the  time  required  to  effect  these  changes  which 
I  have  briefly  described,  it  is  undetennined. 

At  my  next  lecture  I  will  describe  the  lesions  of  the  cir- 
rhotic  kidney. 


LECTURE    XXXIX. 


BEIGHT'S  DISEASES. 

Oirrhotic  or  Gouty  Form,  (Morbid  Anatomy). — Parenchymatous  Nephritis, 
(Etiology  and  Symptoms). 

I  SHALL  this  morning  invite  your  attention  first  to  the 
more  prominent  anatomical  changes  which  are  to  be  found 
in  kidneys  that  are  the  seat  of  the  cirrhotic  form  of  Bright' s 
disease. 

In  this  form  of  Bright' s  disease  the  morbid  processes  do 
not  pass  through  distinct  stages.  It  is,  perhaps,  possible  to 
recognize  anatomically  a  first  and  second  stage,  that  is,  a 
stage  in  which  there  is  an  increase  in  the  intertubular  tissue, 
and  a  stage  of  shrinking  and  atrophy  ;  but  it  is  hardly  pos- 
sible to  recognize  these  divisions  by  any  distinctive  symp- 
toms during  life,  and  you  will  rarely  meet  with  kidneys 
which  after  death  only  present  an  increase  in  the  intertubu- 
lar structure.  The  changes  which  occur  in  the  kidneys  in 
this  form  of  Bright' s  disease  consist  essentially  in  an  in- 
crease in  the  intertubular  structure,  and  a  consequent 
atrophy  of  all  the  other  structures. 

MOEBID  ANATOMY. — Kidneys  which  are  the  seat  of  this 
form  of  disease  will  not  at  first  be  very  much  increased  in 
size  ;  but  as  the  process  progresses,  a  result  is  obtained  similar 
to  that  described  as  occurring  in  the  lung  when  that  organ  is 
the  seat  of  fibrous  induration,  namely,  shrinking  of  tissue. 

As  you  examine  a  kidney  in  which  the  anatomical  changes 
are  well  developed,  you  will  notice  that  the  organ  is  some- 
what diminished  in  size,  and  that  the  capsule  is  thickened 
and  very  adherent ;  the  thickening  of  the  capsule  is  quite 

30 


466  CIRKITOTIC   KIDNEY. 

characteristic,  and  there  is  more  or  less  prolongation  of  the 
connective  tissue  from  the  capsule  into  the  cortical  sub- 
stance. In  consequence  of  these  connective-tissue  prolonga- 
tions, more  or  less  of  the  kidney  structure  will  be  re- 
moved when  the  capsule  is  torn  off,  leaving  the  surface  of 
the  organ  uneven  and  ragged.  After  the  removal  of  the 
capsule,  dilated  veins  are  sometimes  seen  upon  the  surface. 
Upon  section,  it  is  found  that  the  diminution  in  size  is  due 
to  decrease  in  the  cortical  substance.  The  cortical  substance 
of  the  kidneys  is  more  markedly  diminished  in  this  than  in 
any  other  form  of  Bright' s  disease  ;  it  will  also  be  noticed 
that  the  blood-vessels  are  more  distinctly  visible  than  in  the 
normal  kidney.  The  Malpighian  tufts,  however,  are  not  as 
distinctly  visible  as  in  the  normal  kidney,  while  the  medul- 
lary portion  retains  very  nearly  the  same  appearance  and 
is  not  markedly  diminished  in  size.  The  principal  change, 
so  far  as  contraction  is  concerned,  takes  place  in  the  cor- 
tical portion.  This  portion  may  be  reduced  to  one-sixth  its 
normal  thickness.  The  shrinking  is  not  only  apparent  in 
the  cortical  substance  beyond  the  bases  of  the  pyramids, 
but  it  will  be  equally  noticeable  as  affecting  the  tissue  be- 
tween the  pyramids. 

Cysts  are  not  unfrequently  found  in  the  cortical  portion, 
and  are  ordinarily  situated  near  its  surface.  These  cysts 
are  of  varying  size,  and  may  be  the  result  of  a  number  of 
changes. 

If  a  microscopical  examination  be  made  early,  while  the 
first  stage  is  present,  the  following  changes  may  be  found. 
Between  and  around  the  Malpighian  tufts  and  uriniferous 
tubules,  there  will  be  an  increase  of  connective-tissue  cells. 
There  is  a  difference  of  opinion  regarding  the  precise  origin 
of  these  cells,  but  their  presence  is  an  established  fact. 
The  kidney  will  probably  be  slightly  increased  in  size  ;  very 
soon,  however,  it  commences  to  shrink ;  as  a  result  of  the 
shrinking,  the  Malpighian  tufts  diminish  in  size,  for  the 
capsule  which  surrounds  them  also  becomes  thickened,  firm, 
and  fibrous,  and  the  shrinking  which  ensues  presses  upon 
the  tufts  themselves.  You  will  also  find  that  the  arteries 
have  become  hypertrophied,  and  their  walls  present  an 


MORBID   ANATOMY.  467 

irregular  outline.  The  firm  dense  mass  of  connective  tissue 
between  the  Malpighian  tufts  completely  obliterates  the 
expanded  uriniferous  tubules,  bringing  the  tufts  much 
nearer  to  each  other  than  in  the  normal  kidney,  but  it  does 
not  as  a  rule  obliterate  them.  The  Malpighian  tufts  are 
sometimes  obliterated,  but  their  obliteration  is  usually  due 
to  the  development  of  cysts  ;  sometimes  the  process  of  new 
connective-tissue  formations  extends  into  the  medullary  por- 
tion, and  more  or  less  shrinking  of  the  pyramids  occurs  as 
the  result.  It  is  usually,  however,  exclusively  confined  to 
the  cortical  portion  of  the  organ. 

The  tubules  do  not  contain  the  sebaceous-looking  material 
described  as  existing  in  the  other  forms.  If  there  is  any 
abnormal  material  present  in  the  tubules  in  an  uncomplicated 
cirrhotic  kidney,  it  will  be  found  to  be  coagulated  fibrin, 
which  will  be  indicated  by  the  presence  of  hyaline  casts 
in  the  urine  ;  all  the  tubular  changes  are  secondary  to  the 
other  changes. 

There  is  a  difference  of  opinion  in  regard  to  the  nature 
of  these  anatomical  changes.  Some  regard  them  as  in- 
flammatory, while  others  are  of  the  opinion  that  the  in- 
tertubular  changes  are  simply  the  result  of  chronic  hyper- 
semia,  and  occur  independent  of  any  inflammatory  pro- 
cess. This  opinion  is  held  by  some  in  regard  to  the  con- 
nective-tissue increase  in  the  liver  in  cirrhosis.  This  class 
of  observers  regard  its  formation,  in  both  instances,  as 
primarily  dependent  upon  the  action  of  alcohol.  This 
form  of  disease,  however,  is  not  confined  to  the  intemper- 
ate, but  is  chiefly  met  with  in  those  persons  who  have  a 
gouty  diathesis  ;  and  in  this  class  of  cases  there  is  usually 
found,  in  addition  to  the  intertubular  changes  which  have 
already  been  referred  to,  a  deposit  of  urate  of  soda  at  vari- 
ous points  in  the  cortical  substance  and  at  the  apices  of  the 
cones.  The  presence  of  these  deposits  is  certain  evidence 
that  the  patient  during  life  was  the  subject  of  a  gouty 
diathesis,  if  not  an  actual  sufferer  from  articular  manifesta- 
tion of  the  disease. 

The  fact  that  it  does  not  altogether  depend  upon  the 
presence  of  alcohol,  and  may  be  developed  in  the  same 


468  ciRimoTic  KIDNEY. 

manner  as  cirrhosis  of  the  liver  is  sometimes  developed, 
namely,  as  the  result  of  an  interference  with  the  circulation 
in  the  organ,  and  the  accumulation  in  the  interlobular 
tissue  of  colorless  blood-globules  or  formative  cells,  may 
give  support  to  the  supposition  that  the  change  does  not 
depend  upon  inflammatory  processes.  It  is,  however,  a 
fact  established  beyond  dispute,  that  increase  of  connective 
tissue  does  occur  in  the  animal  economy  as  the  result  of 
inflammatory  irritation.  Such  a  development  of  interstitial 
tissue  is  of  common  occurrence  in  the  lungs,  and  is  unques- 
tionably present  in  the  atrophied  stage  of  parenchymatous 
nephritis.  Therefore,  there  can  be  no  possible  objection  to 
the  theory  that  the  inflammatory  process  is  the  principal 
or  only  cause  of  the  anatomical  changes  which  occur  in  this 
form  of  kidney  disease. 

The  cirrhotic  kidney  will  rarely  be  met  with  unassociated 
with  other  degenerative  processes.  The  same  may  be  said 
of  all  forms  of  Bright' s  disease.  You  will  rarely  meet 
with  an  amyloid  kidney  which  is  altogether  waxy.  Any 
form  of  kidney  degeneration  may  be  engrafted  upon  any 
other  form  ;  as,  for  instance,  a  cirrhotic  change  may  be  de- 
veloped upon  a  tubular  inflammation— a  tubular  inflamma- 
tion upon  an  amyloid  or  a  cirrhotic  degeneration.  Indeed, 
a  great  source  of  confusion  in  all  forms  of  Bright' s  disease, 
is  the  change  in  the  tubules,  which  for  the  most  part  are 
inflammatory  in  their  nature.  At  an  autopsy,  the  evidences 
of  amyloid  and  cirrhotic  degeneration  may  be  present  in 
the  kidneys,  and  in  addition,  in  a  large  proportion  of  cases, 
there  will  be  found  evidences  of  recent  tubular  inflamma- 
tion, which  may  have  been  the  direct  cause  of  death. 
Under  such  circumstances,  the  tubular  inflammation  is 
secondary  to  the  cirrhotic  or  amyloid  degeneration, 

Some  claim  that  there  are  no  changes  in  the  amyloid  kid- 
ney which  are  not  secondary  to  tubular  inflammation,  but 
this  is  contrary  to  all  analogy  concerning  amyloid  degenera- 
tion as  affecting  other  organs  ;  and  it  can  hardly  be  possible 
that  the  kidney  should  form  such  a  notable  exception,  and 
that  its  blood-vessels  should  fail  to  be  the  primary  seat  of 
its  development. 


ETIOLOGY.  469 

In  conclusion  I  will  state,  that  although  as  YOU  examine 
a  kidney  which  is  the  seat  of  the  combined  forms  of  degen- 
eration that  we  have  been  considering,  you  will  sometimes 
find  it  difficult  to  determine  the  primary  seat  of  the  lesion, 
yet.  when  yon  take  the  etiology  and  clinical  history  in  con- 
nection with  these  anatomical  changes,  there  will  be  little 
difficulty  in  settling  the  question. 

Having  given  you  an  outline  of  the  anatomical  changes 
which  occur  in  the  three  forms  of  kidney  disease  which  are 
classed  under  the  general  term  of  Bright" s  diseases,  I  will 
return  to  the  history  of  parenchymatous  nephritis,  by  invit- 
ing your  attention  to  its  causation. 

ETIOLOGY  OF  PAREXCIIYMATOUS  NEPHRITIS. 

The  causation  is  the  most  important  part  of  the  history 
of  every  disease  ;  particularly  is  this  true  of  the  one  under 
consideration. 

The  most  common  cause  of  parenchymatous  nephritis, 
especially  in  the  adult,  is  exposure  of  the  surface  to  sud- 
den changes  of  temperature.  This  is  known  from  the  class 
of  subjects  in  which  the  disease  is  most  liable  to  occur,  it 
being  more  frequently  met  with  among  bakers,  firemen, 
moulders,  and  that  class  of  persons  whose  occupation  sub 
jects  them  to  sudden  and  repeated  changes  of  temperature. 
Again,  it  occurs  among  those  who  are  addicted  to  the  use 
of  alcohol ;  they  may  not  be  habitual  drinkers,  or  greatly 
intemperate,  but  they  occasionally  ikgo  on  a  spree,"  and 
while  in  a  state  of  intoxication  expose  themselves  to  sudden 
changes  of  temperature,  or  to  prolonged  cold  after  violent 
exercise.  Under  these  circumstances,  it  is  not  the  alcohol 
that  develops  the  tubular  inflammation,  but  it  is  the  sudden 
changes  of  temperature  to  which  these  persons  subject 
themselves  as  the  legitimate  result  of  such  indulgence.  The 
daily  use  of  alcohol  may  be  indulged  in  for  many  years 
without  the  development  of  this  form  of  kidney  disease, 
provided  the  individual  exercises  care  in  regard  to  expo- 
sure :  alcohol,  therefore,  cannot  be  included  among  the 
direct  causes  of  this  form  of  Bright' s  disease. 

Occasionally  it  happens  thai  a  very  trilling  exposure  tc 


470  PAKE^CHYMATOUS   NEPHEITIS. 

sudden  changes  in  temperature  is  sufficient  to  develop  it, 
such  as  sitting  in  a  draught  of  air  and  exposing  the  loins 
lightly  covered  to  a  current  of  cold  air  while  the  individual 
is  in  a  heated  condition.  In  this  climate  the  failure  to  wear 
flannel  next  the  body  throughout  the  year  is  done  at  the 
risk  of  developing  at  some  time  an  inflammatory  process  in 
the  uriniferous  tubules.  We  do  not  know  with  certainty 
how  this  exposure  acts.  Some  claim  that  chilling  the  sur- 
face of  the  body  causes  congestion  of  the  internal  organs, 
and  as  the  result  of  the  congestion  developed  in  the  kidneys, 
nephritis  occurs.  If  this  theory  is  correct,  the  patient  who 
has  "  chills  and  fever"  should  have  renal  disease  developed 
as  a  consequence,  for  there  is  certainly  a  congestion  of  all 
the  internal  organs  during  the  cold  stage  of  an  intermit- 
tent, but  we  have  no  evidence  that  such  chills  produce 
nephritis. 

There  is  another  theory,  that  the  defective  action  of  the 
skin  which  occurs  when  the  surface  of  the  body  is  exposed 
to  cold,  its  power  of  elimination  being  more  or  less  arrested, 
causes  certain  excrementitious  matters  to  accumulate  in 
the  blood,  and  the  labor  of  the  elimination  of  this  excre- 
mentitious material  is  thrown  upon  the  kidneys,  and  this 
leads  to  irritation  and  inflammation  of  the  uriniferous 
tubules.  There  is  little  doubt  but  that  the  disease  is  some- 
times produced  in  this  way. 

Again,  there  is  another  theory  which  is  quite  reasonable, 
namely,  that  the  nephritic  inflammation  is  due  to  the  reflex 
influence  of  the  nervous  system,  there  being  a  connection 
between  the  sympathetic  nervous  system  and  the  surface  of 
the  body.  This  theory  rests  on  the  same  basis  which  is  em- 
ployed to  explain  the  occurrence  of  pneumonia  and  bron- 
chitis after  exposure  to  cold. 

A  combination  of  the  two  last  theories  will  perhaps  account 
for  the  mode  of  its  development  in  the  largest  proportion  of 
cases.  If,  in  addition  to  the  extra  work  thrown  on  the  kid- 
neys, there  is  a  peculiar  shock  communicated  to  the  general 
system  through  the  sympathetic  nerves,  in  obedience  to  in- 
fluences acting  directly  upon  the  kidneys,  the  condition  is 
favorable  to  the  development  of  renal  tubular  inflammation. 


ETIOLOGY.  471 

Another  very  common  cause  of  this  form  of  Bright' s  dis- 
ease is  the  circulation  of  morbid  elements  in  the  blood,  such 
as  induce  blood-poisoning.  These  poisonous  elements  are 
very  numerous.  Under  this  head  are  embraced  all  those 
poisons  which  give  rise  to  specific  forms  of  fever,  such  as 
scarlatina,  typhus,  diphtheria,  measles,  pyaemia,  rheuma- 
tism, etc.,  etc. 

These  poisons  are  especially  liable  to  develop  tubular 
nephritis,  for  they  act  as  direct  irritants  upon  the  tubuli 
uriniferi.  The  poison  of  scarlet  fever  is  one  of  the  most 
frequent  causes  of  this  form  of  Bright' s  disease.  Every 
epidemic  of  scarlatina  is  not  attended  by  renal  complica- 
tions, for  there  are  some  seasons  when  scarlatina  prevails, 
in  which  scarcely  a  case  of  renal  disease  will  occur ;  while 
during  other  seasons,  almost  every  case  will  be  followed 
by  more  or  less  severe  tubular  inflammation,  and  the  epi- 
demic of  scarlatina  may  apparently  be  no  more  severe  in 
character.  Such  variations  can  only  be  accounted  for  by 
regarding  the  occurrence  of  the  tubular  inflammation  as 
dependent  upon  a  difference  in  the  type  of  the  scarlatina 
poison. 

Another  class  of  causes  of  this  form  of  kidney  disease  may 
be  included  under  the  head  of  renal  irritants,  which  may  be 
introduced  into  the  stomach ;  among  these  are  the  balsam 
of  copaiba,  spirits  of  turpentine,  cantharides,  etc.  The 
prolonged  use  of  these  remedies,  or  their  administration  in 
overdoses,  not  unfrequently  gives  rise  to  tubukir  inflamma- 
tion of  the  kidneys. 

Another  cause  of  nephritis  which  may  be  named,  is  acute 
internal  inflammation,  especially  inflammation  of  the  lungs  ; 
you  should  always  be  on  the  watch  for  its  occurrence  during 
a  severe  pneumonia. 

Still  another  cause  of  renal  tubular  inflammation  is  preg- 
nancy. It  was  formerly  supposed  that  pregnancy  produced 
Bright' s  disease  by  interference  with  the  renal  circulation 
as  the  result  of  pressure  on  the  renal  veins  ;  but,  probably, 
this  is  rarely  a  cause  of  tubular  inflammation.  During 
pregnancy  there  is  an  abnormal  quantity  of  excrementitious 
material  to  be  carried  out  of  the  system  by  the  kidneys, 


472  PAHENCHYMATOUS   JSTEPHKITIS. 

which  not  only  calls  upon  these  organs  for  increased  labor, 
but  this  material  acts  as  an  irritant  to  the  uriniferous  tubes, 
and  the  development  of  tubular  inflammation  is  the  result. 
It  may  occur  at  any  period  of  pregnancy,  but  it  is  rare  be- 
fore the  third  month,  and  is  of  more  frequent  occurrence 
during  the  latter  months.  In  connection  with  pregnancy, 
this  form  of  Bright' s  disease  does  not  usually  pass  beyond 
the  first  stage.  It  often  disappears  rapidly,  and  never  re- 
curs, or  it  may  appear  in  successive  pregnancies,  and  finally 
pass  on  to  the  stage  of  atrophy. 

Again,  passive  congestion  of  the  kidneys  dependent  upon 
interference  with  the  return  circulation,  resulting  from  car- 
diac or  pulmonary  disease,  may  give  rise  to  this  form  of 
Bright' s  disease,  the  anatomical  lesions  of  which  were 
described  under  the  head  of  catarrh  of  the  uriniferous 
tubes. 

There  is  a  degeneration  of  the  epithelium  of  the  urinifer- 
ous tubes,  which  occurs  under  certain  circumstances  inde- 
pendent of  inflammation.  It  is  not  amyloid;  it  is  not,  strictly 
speaking,  a  fatty  change  ;  but  it  occurs  during  the  decay 
processes  of  old  age.  This  epithelial  degeneration  of  the 
uriniferous  tubules  is  a  result  of  senile  change.  In  this 
sense,  extreme  old  age  may  be  regarded  as  a  cause  of  tubular 
epithelial  degeneration  in  the  kidneys. 

Unquestionably,  the  majority  of  cases  of  parenchymatous 
nephritis  commence  as  more  or  less  acute  affections.  The 
acute  symptoms  may  be  of  short  duration,  and  even  over- 
looked by  the  patient ;  but  the  inflammatory  tubular  change 
must  precede  the  degeneration,  and  the  general  condition  of 
the  individual  at  the  time  of  the  primary  changes,  as  well 
as  the  causes  which  may  give  rise  to  their  development,  will 
modify  to  a  very  great  extent  the  rapidity  of  these  changes. 

SYMPTOMS. — We  are  now  brought  to  the  consideration  of 
the  symptoms  of  this  form  of  Bright' s  disease.  I  shall  con- 
sider them  as  far  as  possible  in  connection  with  the  different 
anatomical  stages  of  the  disease. 

Before  proceeding  to  detail  these  symptoms,  let  me  remind 
you  that  the  presence  of  urea  in  the  blood  in  abnormal 
quantities  has  very  much,  if  not  entirely,  to  do  with  the 


SYMPTOMS.  473 

phenomena  which  attend  the  development  of  the  different 
forms  of  Bright' s  disease. 

The  direct  effects  of  an  excess  of  urea  in  the  circulation, 
and  the  different  theories  in  regard  to  its  poisonous  elements, 
I  have  already  considered  under  the  head  of  acute  uraemia. 

The  first  symptom  which  ordinarily  attracts  the  attention 
of  a  patient  in  the  first  stage  of  parenchymatous  nephritis, 
is  oedema  of  the  face.  There  may  have  been  some  symp- 
toms of  gastric  disturbance  prior  to  the  occurrence  of  the 
oedema,  but  they  have  not  been  distinctive  in  their  char- 
acter. After  exposure  to  sudden  and  extreme  variations  in 
temperature,  or  after  an  attack  of  scarlet  fever,  diphtheria, 
or  some  acute  febrile  affection,  or  without  any  known 
cause,  an  individual  notices  a  slight  puffmess  about  the 
eyes  in  the  morning  on  rising  ;  if  he  is  anaemic,  the  oedema 
may  appear  in  the  feet  and  ankles  at  the  same  time.  This 
oedema  usually  increases  very  rapidly.  With  the  occur- 
rence of  the  oedema,  there  is  generally  a  restlessness  which 
cannot  be  accounted  for  by  the  patient.  At  the  same  time 
there  is  more  or  less  rise  in  temperature,  and  these  patients 
will  complain  of  a  constant  headache,  which  seems  to  in- 
crease in  severity  from  hour  to  hour  ;  at  times  the  patient 
is  very  drowsy. 

If  the  patient  is  closely  questioned,  he  will  state  that 
recently  he  has  noticed  some  change  in  his  urine ;  that  it 
has  been  scanty  and  high-colored,  and  he  has  had  frequent 
desire  to  pass  urine.  Perhaps  he  has  had  some  pain  in 
the  back  and  along  the  loins,  and  he  may  also  complain  of 
dyspeptic  symptoms,  some  nausea,  and  perhaps  vomiting, 
which  sometimes  is  a  very  troublesome  symptom,  so  much 
so,  that  the  physician  will  direct  his  attention  to  the 
stomach,  as  the  seat  of  all  the  trouble,  and  treat  the 
patient  for  some  gastric  disease.  There  is  more  or  less  ac- 
celeration of  the  pulse,  which  is  irritable  in  character.  The 
skin  is  usually  unnaturally  dry  ;  occasionally  it  is  moist,  but 
when  it  is  so,  the  perspiration  has  a  peculiar  urinous  odor. 

This  is  a  brief  description  of  the  objective  symptoms 
whicli  attend  the  development  of  the  first  stage  of  a  mild 
form  of  parenchymatous  nephritis.  With  these  symptoms 


474  PAKEXCHYMATOUS   NEPHKITIS. 

you  are  to  expect  notMng  more  than  a  simple  catarrh  of  the 
uriniferous  tubes. 

In  a  favorable  case,  after  the  patient  has  reached  the  con- 
dition described,  he  begins  to  improve  ;  the  urine  is  increased 
in  quantity,  the  oedema  gradually  disappears,  the  headache 
moderates,  the  dyspeptic  symptoms  abate,  and  in  the  course 
of  two  or  three  weeks  the  patient  has  entirely  recovered. 

In  a  certain  proportion  of  cases  no  such  favorable  issue 
occurs.  Instead  of  improving,  the  patient  steadily  grows 
worse  ;  the  oedema  is  present  not  only  in  the  face  and  lower 
extremities,  but  extends  over  the  entire  body.  All  the 
cellular  tissues  of  the  body  become  O3dematous,  externally 
and  internally.  As  the  result  of  the  pulmonary  oedema, 
we  have  dyspnoea.  Dyspnoea  in  this  connection  is  not 
always  dependent  upon  an  oedematous  condition  of  the  lung, 
for  there  is  such  a  thing  as  uraemic  dyspnoea,  independent  of 
any  change  in  the  lung-tissue.  But,  when  the  general  ana- 
sarca  just  described  is  present,  you  will  probably  find  the 
lungs  oedematous.  The  pulmonary  oedema  may  also  some- 
times be  accompanied  by  more  or  less  pulmonary  conges- 
tion, giving  a  watery  expectoration,  which  may  be  streaked 
with  blood.  If  the  disease  progresses,  the  anasarca  will 
gradually  increase  until  the  patient  becomes  perfectly 
"water-logged."  With  the  general  anasarca,  the  surface 
of  the  body  assumes  a  peculiar  pale,  waxy  appearance  ; 
there  is  oedema  of  the  scrotum  and  penis,  and  more  or 
less  effusion  into  the  abdominal  and  thoracic  cavities. 
The  blood  becoming  more  and  more  poisoned  by  the  excre- 
mentitious  matter  which  the  diseased  kidneys  are  unable  to 
eliminate,  a  series  of  nervous  phenomena  are  developed  ;  the 
patient  becomes  very  restless,  muscular  twitchings  are  de- 
veloped, and  these  may  soon  be  followed  by  convulsions, 
coma,  and  death. 

If  this  class  of  patients  do  not  die  from  the  direct  effect 
of  the  urea  upon  the  nerve-centres,  they  may  have  second- 
ary affections,  such  as  meningitis,  pericarditis,  endocarditis, 
pneumonia,  etc.,  which  may  very  rapidly  terminate  fatally. 
This  is  the  most  unfavorable  of  all  the  types  of  parenchy- 
matous  nephritis.  Cases  of  this  type  often  follow  scarlet 


SYMPTOMS.  475 

fever,  and  not  unfrequently  their  severity  is  such  that  they 
do  not  yield  to  any  plan  of  treatment  which  may  be 
adopted.  The  same  type  of  cases  is  also  met  with  in  con- 
nection with  other  diseases  in  which  morbid  changes  in  the 
blood  occur  similar  to  those  which  are  present  in  scarlet 
fever,  a  list  of  which  I  give  you  under  the  head  of  etiology 
of  the  disease. 


LECTURE    XL. 


BRIGHT' S  DISEASES. 

Parenchymatous  Nephritis. — Symptoms. 

WE  have  studied  the  symptoms  of  the  first  stage  of 
parenchymatous  nephritis,  and  I  have  already  described  to 
you  two  types  of  this  stage  of  the  disease  ;  a  very  mild 
type,  which  generally  terminates  in  complete  recovery,  and 
a  very  severe  type,  which  is  usually  rapidly  fatal. 

I  will  this  morning  briefly  detail  the  objective  phenomena 
of  one  or  two  other  types  of  this  stage  of  Bright' s  disease, 
then  carefully  study  a  few  of  its  more  prominent  symp- 
toms. 

The  type  of  cases  to  which  I  wish  especially  to  invite 
your  attention,  includes  those  in  which  the  disease  com- 
mencing either  with  acute  symptoms,  or  stealing  on  insidi- 
ously, does  not  terminate  in  complete  recovery  or  death,  but 
becomes  chronic.  If  its  advent  is  marked  by  acute  symp- 
toms, it  is  attended  by  such  phenomena  as  have  already 
been  detailed ;  the  patient  rapidly  reaches  the  condition  of 
general  anasarca,  which  is  attended  by  IE  :re  or  less  pulmo- 
nary oadema  ;  his  symptoms  are  distressing  and  perhaps 
urgent ;  he  has  probably  reached  the  fourth  or  fifth  week 
of  his  disease  ;  his  countenance  has  assumed  a  very  pallid 
appearance ;  the  pallor  is  not  like  the  clear  pallor  of  phthisis, 
nor  like  the  dingy  pallor  of  cancer,  but  is  peculiar,  not 
easily  described,  is  characteristic  of  this  form  of  Bright' s 
disease,  and  is  easily  recognized  after  having  been  once 


SYMPTOMS.  477 

seen.  Now,  you  probably  have  become  very  anxious  as  to 
the  result  of  the  case ;  but  in  this  almost  hopeless  condi- 
tion, the  patient  begins  to  pass  a  larger  quantity  of  urine  ; 
it  is  sparingly  increased  at  first,  and  perhaps  the  increase  is 
due  to  the  effect  of  remedies  which  you  have  been  employ- 
ing ;  the  appetite  begins  to  return,  nausea  gradually  disap- 
pears ;  the  patient  suffers  less  from  restlessness  ;  the  ana- 
sarca  gradually  diminishes,  the  sleep  becomes  quiet  and  re- 
freshing— in  fact,  there  is  a  gradual  but  steady  improve- 
ment in  all  the  symptoms.  A  patient  in  such  a  condition 
is  passing  from  the  first  into  the  second  stage  of  parenchy- 
matous  nephritis,  and  is  hastening  on  to  the  third  stage. 
The  improvement  which  has  commenced  may  be  con- 
tinued, or  the  patient  may  be  the  subject  of  relapses ;  but 
after  a  few  weeks,  or  perhaps  months,  he  may  be  so  much 
restored  as  to  regard  himself  in  a  comparatively  good  con- 
dition of  health.  Usually,  this  class  of  patients  do  not  so 
far  recover  but  that  they  still  carry  traces  of  the  disease 
with  them  ;  they  reach  the  condition  of  confirmed  invalids, 
never  quite  reaching  the  condition  of  perfect  health.  There 
will  always  remain  some  oedema,  it  never  entirely  disap- 
pears, and  this  is  the  peculiarity  of  this  form  of  Bright' s 
disease.  The  oedema  can  always  be  detected  by  pressing 
firmly  along  the  line  of  the  tibia,  or  behind  the  internal 
malleolus.  and  the  pit  which  is  made  by  firm  pressure  of 
the  finger  indicates  oedema  of  the  cellular  tissue.  Patients 
in  such  a  condition  are  always  inspired  with  the  hope  that 
they  will  reach  complete  recovery. 

When  this  type  of  tubular  nephritis  comes  on  insidiously, 
without  the  occurrence  of  any  very  active  symptoms,  one 
of  the  earliest  symptoms  being  increased  frequency  of 
micturition,  the  oedema  is  never  very  marked,  but  is  always 
present  to  a  limited  degree ;  perhaps  there  is  at  no  time  any 
pain  in  the  back  or  loins  ;  but  there  is  a  time,  early  in  the 
history  of  the  disease,  when  the  urine  is  scanty  and  high- 
colored  ;  afterward  it  becomes  copious,  of  a  pale  color  and 
low  specific  gravity. 

The  gastric  and  nervous  symptoms,  so  prominent  in  the 
other  types  which  I  have  described,  are  present,  but  they 


478  PAREXCHY1IATOITS   NEPHRITIS. 

are  never  severe.  As  the  renal  degenerative  process  ad- 
vances, there  is  gradual  loss  of  energy  and  emaciation  ;  the 
skin  becomes  dry  and  harsh,  the  surface  assumes  a  peculiar 
pale,  sallow  appearance,  there  is  often  great  thirst,  and  if 
you  do  not  see  the  patient  until  the  disease  is  far  advanced, 
you  will  be  very  likely  to  suspect  the  existence  of  diabetes. 

AVhen  this  type  has  reached  the  stage  of  atrophy,  the 
symptoms  are  not  essentially  different  from  those  which  are 
present  in  the  stage  of  atrophy  in  the  other  types  of  this 
disease. 

There  is  still  another  class  of  cases,  or  a  type  of  this  form 
of  disease,  which  is  occasionally  met  with,  of  which  I  will 
say  a  few  words  ;  it  is  a  very  acute  parenchymatous  inflam- 
mation, which  is  ushered  in  by  violent  symptoms,  more 
violent  than  in  either  of  the  classes  to  which  I  have  referred. 
The  patient  is  seized  with  a  chill,  intense  pain  in  the  back 
and  along  the  ureter,  with  retraction  of  both  testicles  ;  there 
is  delirium,  great  disturbance  of  the  nervous  system,  and  an 
array  of  urgent  symptoms.  The  patient  may  pass  into  a 
state  of  coma,  and  die  within  two  or  three  days  from  the 
commencement  of  the  attack.  The  chill  in  these  cases  is 
followed  by  high  temperature,  ranging  from  104°  F.  to 
106°  F.,  almost  complete  suppression  of  urine,  perhaps  not 
more  than  two  ounces  is  secreted  in  twenty-four  hours  ;  the 
delirium  which  is  present  so  closely  resembles  that  of  men- 
ingitis, that  a  differential  diagnosis  is  to  be  made  between 
these  two  conditions. 

In  this  class  of  cases  there  is  a  more  intense,  active  renal 
congestion  than  in  either  of  the  other  types  which  I  have 
described,  and  the  tubules  are  more  completely  and  exten- 
sively filled  with  inflammatory  exudation.  Yery  soon  after 
the  accession  of  the  ushering-in  symptoms,  oedema  of  the 
face  will  be  developed  ;  and  very  soon  after  the  occurrence 
of  the  oedema,  the  patient  will  pass  into  a  state  of  coma 
which  is  usually  followed  by  death. 

If  patients  recover  from  this  acute  form,  they  almost 
invariably  recover  with  permanently  damaged  kidneys,  and 
afterward  present  the  symptoms  of  the  second  and  third 
stage  of  the  disease 


SYMPTOMS.  479 

As  briefly  as  possible,  I  have  given  you  a  general  outline 
of  the  clinical  history  of  the  inflammatory  form  of  Bright' s 
disease.  Connected  with  its  history,  however,  there  are 
symptoms  which  are  of  special  importance,  and  which  I  shall 
consider  more  in  detail ;  these  are,  the  changes  in  the  urine, 
tlie  dropsy,  and  the  nervous  pJienomena.  These  are  present 
to  a  greater  or  less  degree  in  all  cases  of  this  form  of  Bright' s 
disease,  and  their  existence  is  necessary  for  its  diagnosis. 

The  urine.  In  the  outline  history  (which  I  have  just 
given  you),  I  stated  that  in  the  first,  or  acute  stage,  the 
urine  is  diminished  in  quantity,  high-colored,  and  some- 
times is  smoky  in  appearance,  especially  in  the  more  acute 
types  of  the  disease,  is  of  high  specific  gravity,  perhaps  as 
high  as  1030. 

When  tested  for  albumen,  from  one-third  to  one-half  of  the 
entire  bulk  of  the  urine  will  coagulate.  In  testing  for  albu- 
men, it  is  well  to  employ  both  heat  and  nitric  acid.  Albu- 
minous urine  is  usually  coagulated  by  heat  below  the  boil- 
ing-point, and  by  nitric  acid.  If  both  of  these  tests  are 
carefully  used,  you  will  rarely  be  led  into  error  ;  but  mis- 
takes are  often  made  when  only  one  of  these  agents  is  em- 
ployed, for  the  reason,  that  heat  alone  will  not  coagulate 
albumen  in  urine  which  is  neutral  or  alkaline;  in  such 
cases,  the  addition  of  nitric  acid  coagulates  and  precipitates 
the  albumen. 

On  the  other  hand,  in  urine  which  is  alkaline,  neutral,  or 
freely  acid,  a  precipitate  of  phosphatic  salts  may  be  thrown 
down  by  boiling,  and  this  may  be  mistaken  for  albumen. 
The  addition  of  a  drop  or  two  of  nitric  acid  immediately 
dissolves  phosphatic  sediment,  and  renders  the  urine  clear. 
It  is  important  then  that  you  use  both  tests,  and  that  heat 
be  first  employed;  then,  both  acid  and  heat. 

The  next  thing  to  be  determined  is,  whether  there  are 
casts  in  the  urine.  If  a  portion  of  the  urinary  sediment  be 
microscopically  examined  at  this  stage  of  the  disease,  casts 
will  be  found,  which  represent  the  exudation  which  I  have 
already  described  as  filling  more  or  less  completely  the 
uriniferous  tubes  ;  these  casts  consequently  vary  somewhat 
in  appearance  and  composition.  Those  which  are  most 


480  PARE-STCIIYMATOUS   NEPHRITIS. 

characteristic  of  this  stage  are  epithelial  casts.  In  simple 
catarrhal  inflammation  of  the  tubes,  there  is  a  shedding  of 
the  epithelium,  then  epithelial  casts  also  entangle  some 
blood-globules  ;  in  the  very  active  forms  of  the  disease 
some  casts  are  entirely  composed  of  coagulated  blood, 
called  blood- casts  ;  casts  of  this  form  and  composition  are 
found  in  no  other  form  of  Bright' s  disease,  not  in  the  amy- 
loid or  cirrhotic  kidney,  unless  they  are  complicated  by 
tubular  inflammation.  In  addition  to  epithelial  and  blood- 
casts,  you  may  find  some  small  and  large  hyaline  casts. 
The  small  hyaline  casts,  as  you  remember,  are  composed  of 
pure  fibrin  poured  out  into  the  central  portion  of  the  urinif  - 
erous  tubes,  the  epithelium  of  which  has  not  been  removed  ; 
the  large  casts  are  found  in  tubes  the  epithelium  of  which 
has  been  removed.  The  diameter  of  the  la.rge  hyaline  casts 
is  sometimes  twice  that  of  the  small  casts. 

In  addition  to  the  casts,  many  scattered  epithelial  cells 
and  blood-globules  may  be  seen.  Small  hyaline  casts  are 
usually  much  more  numerous  than  large  ones. 

If  you  have  a  patient  who  has  headache,  some  fever,  more 
or  less  oedema,  nausea,  and  perhaps  vomiting,  with  scanty, 
high-colored  urine  of  high  specific  gravity,  containing  epi- 
thelial and  small  hyaline  casts,  and  perhaps  blood-casts  or 
blood-globules  mingled  with  them,  you  may  be  certain  that 
your  patient  is  in  the  first  stage  of  parenchymatous  neph- 
ritis. There  may  be  other  pathological  conditions  existing 
in  the  kidneys  at  the  same  time,  but  the  train  of  phenomena 
just  mentioned  gives  unmistakable  evidence  that  some  of 
the  urinif  erous  tubes  are  the  seat  of  acute  tubular  inflam- 
mation— this  may  be  engrafted  upon  a  chronic  condition. 
In  every  case  of  Bright' s  disease  which  presents  this  line  of 
symptoms,  frequent  examinations  of  the  urine  should  be 
made. 

After  this  stage  of  parenchymatous  nephritis  has  lasted  a 
month  or  six  weeks,  you  will  find  in  adults,  more  rarely  in 
children,  that  oil-globules  begin  to  appear  in  the  renal  casts  ; 
that  the  urine  becomes  more  abundant,  is  not  so  high- 
colored,  its  specific  gravity  is  lower,  and  it  contains  less 
albumen,  not  more  than  one-third  coagulating.  These 


SYMPTOMS.  481 

changes  may  be  regarded  as  evidences  that  the  patient  is 
passing  into  the  second  or  fatty  stage  of  the  disease. 

In  addition  to  those  casts  which  have  jnst  been  described, 
fatty  casts  will  be  present.  The  appearance  of  oil-casts  and 
cells  in  the  urine  indicates  that  the  secreting  cells  and  in- 
flammatory exudations  are  undergoing  fatty  transformation. 

The  patient  is  now  in  the  second  stage  of  parenchymatous 
nephritis.  If  fatty  casts  are  found  in  the  urine  for  any 
length  of  time,  although  recovery  is  possible,  it  does  not 
usually  occur,  but  the  disease  progresses  and  the  stage  of 
atrophy  commences. 

The  urine  is  now  markedly  increased  in  quantity,  it  may 
become  very  abundant,  its  high  color  disappears  and  it 
becomes  pale,  its  specific  gravity  is  sometimes  as  low  as 
1010,  and  although  albumen  is  never  entirely  absent  for  any 
length  of  time,  yet  it  is  very  much  less  in  quantity  than  in 
either  of  the  preceding  stages. 

The  major  portion  of  the  casts  now  found  are  the  large 
hyaline  and  fine  granular  casts ;  the  latter  will  sometimes 
retain  their  epithelial  character,  but  the  epithelium  will 
have  undergone  a  fine  granular  degeneration.  The  existence 
of  fine  granular  casts,  or  large  hyaline  casts,  accompanied 
by  a  free  discharge  of  urine  with  a  low  specific  gravity,  is 
evidence  that  the  patient  has  passed  into  the  third  stage  of 
this  form  of  Bright' s  disease. 

It  is  also  important  in  all  the  three  stages  of  kidney  de- 
generation which  we  have  been  considering,  to  make  a  quan- 
titative analysis  of  the  urine.  There  is  some  difficulty 
attending  such  an  analysis,  for  the  reason  that  as  yet  we 
are  unable  to  determine  how  much  urea  can  be  retained  in 
the  circulation  without  giving  rise  to  serious  disturbance. 
In  some  patients  the  normal  quantity  of  the  urea  in  the 
blood  may  be  very  much  increased,  and  still  the  patient 
suffer  no  inconvenience ;  while  in  others,  a  very  slight 
increase  will  cause  great  disturbance. 

As  our  knowledge  increases  in  respect  to  the  amount  of 
urea  that  can  safely  be  retained  in  the  circulation,  so  will 
the  importance  of  a  quantitive  analysis  of  the  urine  in- 
crease ;  still,  with  our  present  knowledge,  it  is  important  to 
31 


482  PAEE^CHYMATOUS  NEPHEITIS. 

make  a  quantitative  as  well  as  a  qualitative  analysis  of  the 
urine,  for  it  will  enable  you  to  make  a  much  more  reliable 
prognosis  if  you  know  how  much  urea  your  patient  is 
eliminating,  as  it  may  suddenly  diminish  in  quantity,  evi- ' 
dencing  that  some  trouble  is  approaching,  which  cannot  be 
recognized  in  any  other  way. 

The  next  symptom  which  requires  special  notice  is  the 
dropsy. 

Dropsy  occurs  early,  and  is  present  in  every  stage  of  this 
form  of  Bright' s  disease.  There  have  been  several  theories 
advanced  in  regard  to  its  cause,  but  there  is  nothing  certain 
concerning  it.  One  theory  is,  that  it  is  due  to  the  sudden 
removal  from  the  body  of  a  large  amount  of  albumen ; 
whereas,  in  the  most  rapidly-developed  dropsies  no  albu- 
men is  carried  out  of  the  body,  for  the  reason  that  the 
patient  passes  little  or  no  urine. 

Another  cause  assigned  for  the  dropsy  is,  that  the  kid- 
neys fail  to  eliminate  the  watery  portion  of  the  blood  in  the 
form  of  urine,  and  that  the  dropsy  occurs  as  the  result  of 
this  retention  of  the  watery  elements ;  yet  very  extensive 
dropsies  occur  while  the  patient  is  passing  more  than  the 
normal  quantity  .of  urine. 

Again,  another  theory  is  advanced,  which  is  by  far  the 
most  reasonable,  that  the  effect  of  the  urea  on  the  capillary 
circulation  is  such  as  to  interfere  with  its  power.  It  is 
evident  that  the  capillary  circulation  in  connection  with 
Bright' s  disease  is  in  some  way  interfered  with,  for  the 
reason  that  in  every  case  in  which  the  disease  reaches  the 
stage  of  atrophy,  more  or  less  extensive  cardiac  hyper- 
trophy is  developed  in  consequence  of  the  obstruction  to  the 
capillary  circulation. 

Again,  it  is  said  that  when  the  dropsy  occurs  in  connec- 
tion with  the  advanced  stages  of  the  disease,  it  occurs  as  a 
consequence  of  the  anaemic  condition  of  the  patient.  The 
anaemic  condition  undoubtedly  contributes  to  the  ease  with 
which  'the  transudation  of  fluid  through  the  walls  of  the 
vessels  takes  place  ;  but  a  patient  may  be  exceedingly  t 
anaemic  and  yet  no  dropsy  be  present,  and  dropsy  very 
often  occurs  before  the  patient  shows  any  evidence  that  he 


SYMPTOMS.  483 

is  in  an  ansemic  condition.  I  regard  dropsy  as  a  necessary 
symptom  of  this  form  of  Bright' s  disease,  but  the  exact 
cause  of  its  occurrence  in  every  case  cannot  be  determined. 
Undoubtedly,  the  most  constant  and  perhaps  the  most 
efficient  cause  is  the  direct  effect  of  the  excess  of  urea  upon 
the  capillary  circulation  and  upon  the  composition  of  the 
blood-.  In  the  early  stage,  the  dropsy  is  a  very  marked  symp- 
tom ;  in  the  stage  of  atrophy  it  may  not  be  very  marked, 
but  there  is  always  some  oedema  of  the  feet  and  ankles. 

I  now  come  to  the  consideration  of  the  nervous  symp- 
toms, which  are  of  great  importance  and  prominence.  Un- 
doubtedly, these  are  due  to  the  presence  of  some  irritating 
poison  in  the  circulation,  which  acts  directly  upon  the 
nervous  system.  Some  have  claimed  that  these  nervous 
phenomena  are  due  to  the  retention  in  the  circulation  of 
all  the  constituents  of  the  urine,  but  it  seems  more  reason- 
able to  suppose  that  urea  is  the  substance  which  gives  rise 
to  the  toxsemic  symptoms. 

The  different  theories  in  regard  to  the  causation  of  these 
symptoms,  I  have  considered  under  the  head  of  acute 
uraemia.  Usually,  the  nervous  symptoms  first  manifest 
themselves  by  headache  ;  therefore  headache  is  a  symptom 
which  must  not  be  lightly  regarded,  for  it  is  often  the  pre- 
cursor of  more  dangerous  symptoms.  If  persistent  and 
severe,  and  permitted  to  pass  unrelieved,  it  may  be  followed 
by  convulsions.  The  larger  proportion  of  cases  in  the  first 
stage  of  this  form  of  Bright' s  disease,  will  suffer  from  head- 
ache, more  or  less  severe,  without  any  subsequent  convul- 
sions ;  but  the  fact  that  convulsions  do  occasionally  follow 
is  sufficient  warning  for  you  to  watch  for  the  indications  of 
convulsions. 

If  the  poisoning  goes  on  gradually,  the  patient  will  first 
become  drowsy,  the  drowsiness  passing  into  stupor,  and 
frequently  he  will  pass  into  a  state  of  coma.  You  will  not 
be  so  apt  to  have  convulsions  as  when  the  poisoning  takes 
place  rapidly. 

A  large  number  of  patients  with  this  form  of  Bright' s 
disease  unquestionably  die  from  the  direct  effect  of  the 
urea  upon  the  nervous  centres  ;  but  a  still  larger  number 


484  PARENCHYMATOUS   NEPHRITIS. 

die  from  the  complications  which  are  developed  during  its 
course. 

By  remembering  the  prominent  points  in  the  history  of 
this  form  of  Bright' s  disease,  to  which  I  have  briefly  called 
your  attention,  you  will  be  able,  in  the  majority  of  in- 
stances, not  only  to  recognize  its  existence,  but  to  deter- 
mine the  stage  of  the  inflammatory  process,  whether,  it  be 
that  of  congestion  and  commencing  exudation,  of  exuda- 
tion and  commencing  degeneration,  or  of  degeneration  and 
atrophy. 

Before  giving  you  the  rules  for  the  differential  diagnosis 
of  this  form  of  Bright' s  disease,  it  will  be  necessary  for  me 
to  speak  of  the  complications  which  are  liable  to  occur  dur- 
ing its  progress,  and  which,  in  many  instances,  modify  to 
a  very  great  extent  its  clinical  history. 

One  of  the  most  constant  complications  of  the  advanced 
stage  of  this  form  of  Bright' s  disease,  is  the  development 
of  cardiac  hypertrophy.  This  complication  will  never  be 
met  with  in  the  first  or  second  stages  of  the  disease,  but 
will  always  be  present  to  a  greater  or  less  degree  in  the 
stage  of  atrophy.  This  hypertrophy  is  due  to  interference 
with  the  systemic  capillary  circulation,  which  results  from 
the  long-continued  excess  of  urea  in  the  blood. 

Its  existence  is  an  evidence  that  the  renal  disease,  of  which 
it  is  a  complication,  has  existed  for  a  considerable  time. 
The  fact  of  its  existence  under  certain  circumstances  may 
be  of  service  in  enabling  you  to  determine  the  stage  of  the 
disease.  For  instance,  you  may  be  called  to  a  patient  who 
is  in  a  condition  of  coma  or  convulsion, — if  you  find  that 
simple  cardiac  hypertrophy  exists,  it  will  enable  you  to 
decide  that  the  patient  is  not  in  the  first  stage  of  the  dis- 
ease, and  that  the  coma  or  convulsions  are  dependent  upon 
an  engrafting  of  an  acute  tubular  inflammation  on  a  chronic 
stage  of  the  disease. 

Complications  affecting  the  lungs  and  bronchi  are  of  quite 
frequent  occurrence.  Prominent  among  these  is  pulmonary 
oedema.  This  may  be  developed  in  connection  with  any 
stage  of  the  disease,  but  it  occurs  most  frequently  in  con- 
nection with  the  first  stage. 


COMPLICATIONS.  485 

Another  very  important  pulmonary  complication  is  pneu- 
monia. The  pneumonia  developed  under  these  circumstances 
usually  progresses  according  to  the  rules  which  govern 
acute  pneumonia.  The  pneumonia  itself  is  not  particularly 
dangerous — but  there  is  danger  from  the  sudden  develop- 
ment of  pulmonary  oedema,  affecting  portions  of  the  lung 
unaffected  by  the  pneumonia.  This  danger  must  be  antici- 
pated, and  means  must  be  employed  to  arrest  its  develop- 
ment on  the  occurrence  of  the  first  symptoms  indicating  its 
presence.  The  mere  presence  of  albumen  in  the  urine  of  a 
patient  suffering  from  pneumonia  is  of  but  slight  signifi- 
cance, but  the  presence  of  casts  in  the  urine  indicating  the 
existence  of  tubular  nephritis  is  an  element  of  danger  not 
to  be  lightly  regarded. 

Bronchitis  is  another  pulmonary  complication  of  this 
form  of  Bright' s  disease.  It  may  occur  as  an  acute  affec- 
tion in  the  first  stage  of  the  kidney  disease,  but  it  is  much 
more  likely  to  occur  as  a  chronic  affection  in  the  advanced 
stage  of  the  disease. 

Inflammation  of  serous  membranes  is  another  class  of 
complications  of  quite  frequent  occurrence  in  parenchyma- 
tous  nephritis. 

The  serous  membrane  most  frequently  affected  is  the 
endocardium.  Your  text-books  say  that  it  is  the  last  com- 
plication likely  to  occur,  but  I  would  place  it  at  the  head 
of  the  list.  The  reason  that  endocarditis  is  of  so  frequent 
occurrence  is,  that  the  endocardial  surface  is  constantly  ex- 
posed to  the  irritating  influence  of  the  poison  contained  in 
the  blood  as  the  result  of  the  arrest  of  the  renal  function. 

The  next  most  frequent  serous  inflammation  occurring  in 
this  connection  is  pleurisy.  The  pleurisy  of  Bright' s  dis- 
ease is  usually  insidious  in  its  development,  and  ordinarily 
occurs  only  in  the  latter  stages  of  the  disease. 

Meningitis  of  Bright' s  disease  is  most  frequently  devel- 
oped in  its  acute  stage.  Another  complication  which  may 
occur  is  subacute  inflammation  of  the  mucous  membrane 
of  the  stomach.  This  mucous  membrane  undergoes  struc- 
tural changes,  and  patients  never  entirely  recover  from 
these  changes. 


486  PARENCHYMATOUS   NEPHRITIS. 

Amaurosis  is  also  a  complication  of  this  form  of  Bright' s 
disease.  There  are  two  forms.  One  occurs  during  the  first 
stage,  the  stage  in  which  there  may  have  been  considerable 
cerebral  disturbance ;  perhaps  the  patient  has  had  convul- 
sions and  coma,  and  when  he  has  somewhat  recovered  from 
these  acute  symptoms  there  may  be  complete  loss  of  sight. 
This  form  of  amaurosis  is  usually  temporary,  and  is  unat- 
tended by  any  change  in  the  retina  recognizable  by  the 
opthalmoscope  ;  it  is  probably  due  to  the  direct  effect  of 
the  urea  upon  the  retina. 

The  other  form  is  first  indicated  by  the  patient's  in- 
ability to  see  distinctly ;  subsequently  he  has  more  or  less 
difficulty  in  reading  print  which  formerly  he  had  read  with 
ease ;  lenses  do  not  improve  his  vision — after  a  time  the 
sight  may  be  entirely  lost. 

This  form  of  amaurosis  is  due  to  an  inflammation  affect- 
ing the  retina — a  neuro-retinitis.  This  is  present  to  a  greater 
or  less  degree  in  a  large  number  of  patients  with  chronic 
Blight's  disease,  and  sometimes  by  opthalmoscopic  exami- 
nation Bright' s  disease  can  be  recognized  from  the  con- 
dition of  the  retina  when  the  other  symptoms  of  the  disease 
have  been  overlooked  or  when  they  are  not  well  marked. 


LECTUEE    XLI. 


BRIGHT' S  DISEASES. 

Parenchymatous    Nephritis   (continued.). — Differential    Diagnosis. — Amyloid 
Degeneration  of  Kidneys;  Etiology,  etc. — Cirrhotic  Kidney ;  Etiology,  etc. 

THIS  morning  I  shall  first  invite  your  attention  to  the 
more  prominent  points  in  the  differential  diagnosis  of  the 
various  stages  of  parenchymatous  nephritis  which  were 
engaging  our  attention  at  my  last  lecture.  The  general 
symptoms  and  the  changes  in  the  urine  in  the  first  stage 
of  this  form  of  Bright' s  disease  are  so  obvious  that  it  can 
scarcely  be  overlooked  or  mistaken  for  any  other  disease. 
The  only  circumstances  under  which  it  is  possible  for  the 
acute  stage  of  this  affection  to  pass  unrecognized  are  those 
in  which  the  dropsy  is  not  a  prominent  symptom,  and  when 
a  careful  examination  of  the  urine  has  not  been  made. 

You  may  not  always  be  able  readily  to  determine  whether 
an  acute  attack  is  primary  or  secondary,  that  is,  whether  it 
has  occurred  in  kidneys  that  were  healthy  at  the  time  of 
its  occurrence,  or  that  were  already  the  seat  of  a  chronic 
degeneration.  The  previous  history  of  the  patient,  and  the 
presence  or  absence  of  cardiac  hypertrophy,  are  the  only 
means  which  you  have  to  guide  you  in  your  decision. 

I  have  already  told  you  that  high-colored,  smoky,  and 
blood-tinged  urine,  of  high  specific  gravity,  containing 
epithelial,  small  hyaline  and  blood-casts,  gives  positive  in- 
dications of  the  acute  stage  of  this  form  of  Bright' s  dis- 
ease ;  but  these  indications  may  all  be  present  when  an 
acute  attack  is  engrafted  upon  a  chronic  degeneration. 


488  DIFFERENTIAL  DIAGNOSIS. 

On  the  other  hand,  when  the  urine  is  abundant,  of  pale 
color,  low  specific  gravity,  highly  albuminous,  and  con- 
tains fatty,  granular  and  hyaline  casts,  it  furnishes  positive 
evidence  of  an  advanced  stage  of  this  form  of  Bright' s  dis- 
ease. 

In  all  cases,  a  careful  consideration  of  the  previous  his- 
tory and  causation  of  the  disease  is  of  great  diagnostic  im- 
portance. 

A  state  of  ursemic  stupor,  with  a  dry  tongue  and  sordes 
on  the  teeth,  may  be  mistaken  for  typhus  or  typhoid  fever, 
yet  the  history  of  the  case,  and  a  careful  examination  of 
the  urine,  will  serve  to  remove  all  doubts.  Bear  in  mind 
that  a  patient  with  chronic  renal  disease  may  also  have  a 
specific  fever,  and  that  patients  with  specific  fever  may  have 
scanty  and  albuminous  urine,  but  it  rarely  if  ever  contains 
casts,  unless  parenchymatous  nephritis  is  present  as  a  com- 
plication. 

The  same  rules  will  also  enable  you  to  make  a  differential 
diagnosis  between  this  form  of  Bright' s  disease  and  pneu- 
monia, erysipelas  and  pyaemia,  when  the  latter  are  attended 
by  scanty,  high-colored,  and  albuminous  urine. 

If  the  urine  is  subjected  to  a  careful  examination,  it  is 
hardly  possible  for  one  to  confound  the  anaemia  and  cachexia 
which  sometimes  attend  the  stage  of  atrophy  in  this  form 
of  renal  disease  with  the  cachexia  of  other  organic  diseases. 

The  mistakes  that  are  made  in  diagnosis,  or  rather  the 
failures  to  recognize  the  existence  of  this  form  of  renal  dis- 
ease, are  usually  due  to  the  fact  that  careful  and  repeated 
examinations  of  the  urine  have  not  been  made.  In  every 
case  of  persistent  dyspepsia  which  does  not  yield  to  treat- 
ment, you  should  carefully  examine  the  urine,  and  you 
will  be  surprised  at  the  frequency  of  the  occurrence  of  dys- 
pepsia with  the  advanced  stage  of  this  form  of  Bright' s  dis- 
ease. 

PROGNOSIS. — Concerning  the  prognosis,  I  have  already 
said  much  in  connection  with  the  history  of  the  complica- 
tions which  are  so  frequent  attendants  of  this  form  of  kid- 
ney disease.  The  tendency  in  the  first  stage  is  to  recovery. 
In  this  stage,  perhaps  it  is  as  curable  a  disease  as  acute 


PARENCHYMATOUS   NEPHRITIS.  489 

bronchitis  or  pneumonia,  but  the  chances  of  recovery  are 
much  better  in  the  young  than  in  persons  passed  middle 
life.  In  those  cases  which  terminate  in  recovery,  the  char- 
acteristic symptoms  of  the  disease  disappear  within  two  or 
three  months  from  the  commencement  of  the  attack ;  the 
albumen  in  the  urine  is  the  last  to  disappear.  So  long  as 
albumen  continues  in  the  urine,  however  small  in  quantity 
it  may  be,  recovery  cannot  be  regarded  as  complete.  Al- 
though the  majority  of  this  class  of  patients  recover,  yet 
not  unfrequently  the  disease  terminates  fatally.  The 
symptoms  which  indicate  a  fatal  termination  are,  very 
scanty  urine,  frequent  and  distressing  vomiting,  extensive 
anasarca,  severe  and  persistent  headache,  convulsions, 
coma,  typhoid  symptoms,  and  the  occurrence  of  any  of  the 
acute  complications  to  which  I  have  referred. 

Again,  in  quite  a  large  proportion  of  cases,  the  patient 
passes  rapidly  from  the  first,  or  acute,  into  the  second  and 
third,  or  chronic  stage  of  the  disease.  The  termination  of 
the  first,  or  acute  stage,  is  indicated  by  a  copious  secretion 
of  urine ;  it  becomes  pale  in  color,  it  still  contains  casts,  but 
they  are  less  in  number,  and  their  character  is  changed  in 
the  manner  already  described.  The  dropsy  diminishes,  but 
does  not  entirely  disappear.  The  patient  may  be  able  to 
return  to  his  ordinary  duties,  but  the  oedema  of  the  feet  and 
ankles  does  not  entirely  disappear,  and  the  urine  remains 
albuminous. 

In  the  advanced  stage  of  parenchymatous  nephritis,  the 
structural  changes  in  the  kidneys  are  such  that  they  do  not 
admit  of  repair.  All  portions  of  the  kidney,  however,  are 
not  equally  affected,  consequently  the  depurative  function 
of  the  organ  is  not  entirely  suspended,  but  is  imperfectly 
carried  on.  So  long  as  the  degenerative  process  is  not  pro- 
gressive, this  class  of  patients  get  along  quite  comfortably, 
but  its  tendency  is  to  progress,  and  more  and  more  of  the 
kidney-tissue  becomes  involved,  until  at  length  it  reaches 
a  point  beyond  which  life  cannot  be  sustained. 

In  a  large  number  of  cases,  long  before  this  limit  is 
reached,  some  one  of  the  numerous  complications  to  which 
I  have  referred  cause  death. 


490  ETIOLOGY. 

In  the  advanced  stage  of  this  form  of  Bright' s  disease, 
the  most  trustworthy  prognostic  indications  are  to  be  ob- 
tained by  comparing  the  evidences  furnished  by  the  urine 
with  the  general  symptoms. 

You  must  always  be  cautions  in  giving  a  prognosis  as 
regards  time,  for  the  symptoms  may  suddenly  be  greatly 
aggravated  by  some  imprudence  on  the  part  of  your  patient. 
From  exposure  to  cold,  or  error  in  diet,  he  may  rapidly 
pass  from  a  condition  of  comparative  good  health  to  the 
verge  of  ursemic  coma  or  convulsions. 

Although  in  all  advanced  cases  of  this  disease  the  prog- 
nosis is  unfavorable,  still  there  is  reason  to  hope  that  by 
judicious  management,  even  in  the  most  unpromising  cases, 
you  may  be  able  to  relieve  many  of  the  more  distress- 
ing symptoms,  and  greatly  prolong  the  life  of  your  pa- 
tient. 

Before  considering  the  plan  of  treatment  to  be  followed 
in  the  management  of  this  form  of  Bright' s  disease,  I  will 
invite  your  attention  to  the  history  of  the  causes  and  symp- 
toms of  the  amyloid  and  cirrhotic  degenerations  of  the 
kidney,  after  which,  under  one  head,  I  shall  detail  the 
treatment  of  these  three  forms  of  disease. 

ETIOLOGY. — I  shall  first  speak  of  the  etiology  of  the  amy- 
loid kidney. 

The  primary  cause  of  amyloid  degeneration  is  still  a 
vexed  question.  It  never  occurs  in  persons  who  are  in 
perfect  health,  and  the  circumstances  under  which  it  almost 
uniformly  occurs,  to  a  certain  extent,  must  determine  its 
causation. 

Amyloid  degeneration  of  the  kidneys  undoubtedly  is 
most  frequently  met  with  in  connection  with  syphilis  in  its 
tertiary  form.  You  may  remember  that  the  statement  has 
been  made  that  this  form  of  kidney  degeneration  rarely 
occurs  unaccompanied  by  amyloid  degeneration  of  other 
organs  and  tissues  of  the  body,  and  these  degenerations 
recognize  syphilis  as  their  principal  cause. 

Another  frequent  cause  of  amyloid  degeneration  is  pro- 
longed suppuration,  especially  when  associated  with  diseases 
of  bone. 


AMYLOID   KIDNEY.  49] 

Just  here  is  an  important  practical  point,  and  that  is, 
never  allow  a  suppuration  to  continue  any  longer  than  is 
necessary  from  the  nature  of  the  case.  It  is  not  wise  to 
wait  any  length  of  time  for  a  spontaneous  opening  in  a  case 
of  empyema  or  deep-seated  abscess.  Do  not  suffer  too  long 
processes  of  necrosis  to  exist,  waiting  for  the  spontaneous 
removal  of  the  necrosed  bone,  nor  hesitate  to  interfere  in 
any  other  suppurative  disease,  when  it  is  possible  to  relieve 
or  remove  the  cause  of  the  suppuration. 

A  too  long-continued  empyema  may  give  as  a  result  an 
amyloid  kidney,  which  will  very  much  complicate  the  case, 
and  be  an  element  of  fatal  termination.  Amyloid  kidney 
is  very  frequently  met  with  in  those  who  die  of  pulmonary 
phthisis,  consequently  chronic  suppurative  diseases  of  the 
lungs  must  be  ranked  among  the  causes  of  this  form  of 
renal  degeneration. 

SYMPTOMS. — The  symptoms  which  attend  the  development 
of  this  form  of  kidney  degeneration  are  never  very  well 
marked,  especially  in  its  early  stage.  The  usual  manner  of 
its  development  is  as  follows  :  an  individual  who  is  suffer- 
ing from  some  exhausting  form  of  disease,  such  as  I  have 
already  alluded  to,  notices  that  he  is  losing  strength,  that 
he  is  becoming  more  feeble  than  usual,  and  that  he  has  less 
mental  and  physical  vigor  than  he  is  accustomed  to  have. 
He  finds  that  he  is  unable  to  accomplish  his  usual  amount 
of  work ;  that  he  is  troubled  with  shortness  of  breath  on 
exertion  ;  that  he  has  an  unusually  pallid  countenance,  and 
that  there  is  a  great  increase  in  the  quantity  of  urine  which 
he  voids  in  the  twenty -four  hours.  He  is  now  obliged  to 
rise  two  or  three  times  during  the  night  to  pass  urine,  and 
at  times  he  passes  large  quantities.  He  also  notices  a  ful- 
ness of  the  abdomen  which  he  has  never  before  observed, 
and  sometimes  there  is  a  sense  of  weight  about  the  upper 
part  of  the  abdomen. 

He  may  have  detected  a  tumor  in  the  right,  and  perhaps 
one  also  in  the  left  hypochoiidrium.  When  he  assumes  the 
recumbent  posture,  on  account  of  the  dyspnoea,  he  must 
have  the  upper  portion  of  the  body  elevated.  Doubtless 
the  dyspnoea  is  partially  due  to  the  anaemic  condition  of 


492  SYMPTOMS. 

the  patient,  and  partially  to  the  upward  pressure  caused  by 
an  enlarged  liver  and  spleen.  Perhaps  there  is  slight 
oedema  about  the  ankles,  especially  at  night.  He  does  not 
perspire  readily,  but  when  he  does,  the  perspiration  has  an 
urinous  odor.  Certain  articles  of  food,  especially  fatty 
substances,  which  never  before  have  disagreed  with  him, 
now  give  rise  to  dyspeptic  symptoms,  and  he  may  have 
occasional  vomitings. 

This  train  of  symptoms,  coming  on  in  a  person  who  has 
been  the  subject  of  any  of  the  forms  of  disease  to  which  I 
have  referred,  leads  one  to  suspect  that  amyloid  degenera- 
tion of  the  kidney  is  taking  place.  If,  upon  further  exam- 
tion,  a  marked  enlargement  of  the  liver  and  spleen  is  found 
(for  the  two  conditions  are  always  associated),  and  the  sur- 
face of  the  liver  is  smooth  and  its  edges  sharp,  you  may  be 
certain  that  the  amyloid  form  of  Bright' s  disease  exists. 
With  these  symptoms  there  will  also  be  more  or  less  fluid 
found  in  the  abdominal  cavity,  but  its  presence  will  be  due 
to  changes  which  have  occurred  in  the  liver,  and  will  not 
depend  upon  the  changes  in  the  kidneys. 

In  this  class  of  patients,  in  a  large  proportion  of  cases, 
there  is  a  peculiar  cachexia  present  which  is  almost  char- 
acteristic. The  patient  has  a  pale,  waxy  complexion,  with 
little  pigmentary  deposits  in  the  skin,  particularly  about 
the  eyelids.  This  cachexia  is  usually  most  marked  in 
syphilitic  subjects. 

In  this  form,  as  in  the  inflammatory  form  of  kidney  dis- 
ease, there  are  three  prominent  classes  of  symptoms.  The 
first  class  includes  those  symptoms  present  with  abnormal 
changes  in  the  urine.  The  second  class  includes  those 
which  we  have  with  dropsy.  The  third  class  includes  those 
which  have  to  do  with  changes  in  the  nervous  system.  It  is 
important  that  we  consider  each  of  these  in  detail. 

The  urine,  as  I  have  already  stated,  is  increased  in  quan- 
tity, the  patient  may  be  passing  as  much  as  one  hundred 
ounces  in  twenty-four  hours  ;  forty  ounces  in  twenty-four 
hours  is  a  small  quantity  to  be  passed  by  a  patient  with 
amyloid  kidneys.  It  is  light-colored,  looking  very  much 
like  clear  water,  or  it  may  have  a  slight  amber  color.  It  is 


AMYLOID   KIDNEY.  493 

of  low  specific  gravity,  sometimes  as  low  as  1005.  When 
tested  for  albumen,  it  will  be  found  always  to  contain  an 
appreciable  quantity.  Usually  the  quantity  is  not  large, 
and  sometimes  the  most  delicate  tests  will  only  give  a  trace, 
but  some  is  invariably  present.  When  the  urine  is  ex- 
amined microscopically,  it  will  be  found  to  contain  casts, 
either  large  hyaline,  or  fine  granular,  or  both.  Casts  of 
either  variety  usually  are  not  abundant,  and  several  ex- 
aminations may  be  required  before  their  presence  or  ab- 
sence can  be  positively  determined.  Epithelial  or  fatty 
casts  may  sometimes  be  found  in  the  urine  of  patients  who 
are  suffering  from  amyloid  degeneration  of  the  kidneys, 
but  their  presence  is  an  indication  that  the  patient  has 
something  more  than  amyloid  kidney,  that  there  has  been 
engrafted  upon  the  amyloid  form  of  the  disease  an  inflam- 
matory process  in  the  tubules.  The  presence  of  a  large 
quantity  of  albumen  in  the  urine  of  a  patient  known  to 
be  suffering  from  amyloid  degeneration  of  a  kidney,  may 
be  regarded  as  almost  positive  evidence  that  tubular  inflam- 
mation has  occurred  in  an  already  degenerated  kidney. 

The  large  quantity  of  urine  voided  by  patients  with 
amyloid  kidney  attracts  attention,  and  not  unfrequently  a 
patient  with  waxy  kidney  will  come  to  you  with  the  idea  that 
he  has  diabetes.  The  quantity  of  urine  passed  is  so  large, 
and  there  is  such  rapid  loss  of  flesh  and  strength,  accom- 
panied by  dyspeptic  symptoms,  with  a  disinclination  to 
exertion,  that  unless  you  are  upon  your  guard  you  will  be 
led  into  the  same  error  of  belief,  but  an  examination  of 
the  urine  will  soon  settle  the  question  whether  the  patient 
is  or  is  not  suifering  from  diabetes.  The  urine  is  of  low 
specific  gravity,  contains  no  sugar,  but  albumen  and  casts 
are  found  in  greater  or  less  abundance. 

With  regard  to  the  dropsy,  it  is  never  very  marked  in 
this  form  of  Bright' s  disease.  The  general  anasarca  which 
is  so  frequently  met  with  in  connection  with  parenchyma- 
tous  nephritis,  is  never  present.  There  may  be  slight 
oadema  of  the  feet,  especially  at  night,  and  you  may  find 
fluid  in  the  abdominal  cavity,  but  the  ascites,  as  I  have 
already  stated,  is  due  to  changes  in  the  liver  rather  than  to 


494  SYMPTOMS. 

changes  in  the  kidney.  If  general  anasarca  is  present  in 
connection  with  waxy  degeneration  of  the  kidney,  it  must 
be  regarded  as  certain  evidence  that  tubular  inflamma- 
tion has  been  engrafted  upon  the  primary  kidney  degenera- 
tion. 

The  nervous  symptoms  which  are  present  in  this  form  of 
Bright' s  disease  are  never  very  prominent.  This  class  of 
patients  do  not  usually  suffer  very  much  from  headache, 
and  rarely  have  convulsions  or  pass  into  coma.  They 
usually  die  from  exhaustion,  or  from  some  complication, 
or  in  other  words  die  as  much  from  the  effects  of  amyloid 
degeneration  of  other  organs  as  from  amyloid  degeneration 
of  the  kidneys.  It  is  a  question  whether  amyloid  degenera- 
tion affecting  only  the  kidneys  ever  proves  fatal.  Diarrhoea, 
the  result  of  amyloid  degeneration  of  the  mucous  mem- 
brane, or  ascites  depending  upon  changes  in  the  liver,  may 
cause  death. 

You  are  not  as  likely  to  meet  with  active  complications  in 
this  form  as  in  the  inflammatory  form  of  Bright' s  disease. 
Most  of  the  complications  which  occur  are  degenerative  in 
character.  Patients  are  not  especially  liable  to  have  pneu- 
monia, bronchitis  or  pericarditis,  or  any  of  the  acute  in- 
flammations occurring  in  connection  with  the  inflammatory 
form. 

If  dyspeptic  symptoms,  which  are  persistent  and  do  not 
readily  yield  to  treatment,  occur  with  amyloid  kidney,  and 
if  with  them  we  have  enlargement  of  the  liver  and  spleen, 
and  if,  besides,  diarrhoea  is  developed,  the  existence  of  amy- 
loid degeneration  of  the  intestines  is  established  almost  be- 
yond a  doubt,  and  it  is  equally  certain  that  the  diarrhoea 
will  destroy  the  life  of  the  patient. 

Cardiac  hypertrophy  does  not  usually  occur  as  a  compli- 
cation with  this  form  of  the  disease,  but  we  expect  to  find 
it  as  such  in  the  stage  of  atrophy  of  parenchymatous  ne- 
phritis and  in  the  cirrhotic  kidney  ;  rarely  is  it  present  in 
any  stage  of  the  amyloid  kidney. 

DIFFERENTIAL  DIAGNOSIS. — In  the  early  stages,  usually 
it  is  not  difficult  to  make  a  differential  diagnosis  between 
the  two  forms  of  Bright' s  disease,  which  have  been  engag- 


AMYLOID   KIDNEY.  495 

ing  our  attention,  unless  the  amyloid  degeneration  ±s  compli 
cated  by  tubular  inflammation.  When  this  is  the  case,  the 
differential  diagnosis  can  only  be  made  by  a  very  careful 
study  of  the  history  of  the  case.  In  either  form,  when  the 
degeneration  has  reached  the  stage  of  atrophy,  it  is  often 
very  difficult  and  sometimes  impossible  to  distinguish  the 
one  from  the  other. 

When  from  the  commencement  of  the  disease  there  has 
been  a  copious  secretion  of  urine  of  low  specific  gravity, 
containing  little  albumen,  and  when  the  symptoms  of  the 
disease  have  come  on  gradually  in  one  who  is  suffering 
from  an  exhausting  disease,  you  may  expect  to  find  amy- 
loid  kidneys,  and  the  probability  of  this  will  be  greatly  in- 
creased if  the  liver  and  spleen  are  found  enlarged. 

It  is  hardly  possible  to  confound  the  cachexia  which 
attends  this  form  of  Bright' s  disease  with  that  of  any  other 
chronic  disease,  for  a  chemical  and  microscopical  examina- 
tion of  the  urine  will  tell  you  positively  that  some  form 
of  renal  disease  exists,  and  it  only  remains  for  you  to 
determine  what  form  of  degeneration  of  the  kidneys  is 
present. 

PROGNOSIS. — The  prognosis  in  this  form  of  Bright' s  dis- 
ease, as  far  as  regards  time,  is  uncertain  it  undoubtedly 
takes  many  years  for  the  anatomical  changes  in  the  kidney 
to  reach  the  stage  of  atrophy,  yet  when  it  is  once  estab- 
lished recovery  is  impossible.  Resulting  as  it  does  from  a 
grave  constitutional  cachexia,  the  causes  which  produce  it  are 
constantly  in  operation,  and  they  are  but  slightly,  if  in  any 
degree  influenced  by  treatment.  The  progress  of  the  dis- 
ease may  be  temporarily  arrested,  but  its  usual  course  is 
one  of  steady  progress  towards  a  fatal  termination. 

An  exhausting  diarrhoea,  or  a  dropsical  accumulation, 
not  the  result  of  changes  in  the  kidneys  but  in  other  organs, 
is  the  immediate  cause  of  death. 

The  early  symptoms  are  often  so  obscure  that  it  is  diffi- 
cult to  determine  the  date  of  the  origin  of  the  disease,  con- 
sequently the  existence  of  amyloid  degeneration  of  the  kid- 
ney is  rarely  recognized  until  the  structural  changes  in  the 
organs  are  far  advanced,  when  it  is  very  liable  to  be  com- 


496  ETIOLOGY. 

plicated  by  tubular  inflammation.  With  the  exception  of 
its  treatment,  these  are  the  principal  points  in  the  history 
of  the  amyloid  form  of  Bright' s  disease.  I  shall  consider  its 
treatment  in  connection  with  the  treatment  of  the  other 
forms  of  this  class  of  diseases. 

Probably  you  will  not  be  able  to  recognize  it  during  its 
first  stage,  but  it  is  readily  recognized  during  its  second  and 
third  stage.  You  may  not  always  reach  a  diagnosis  by  an 
examination  of  the  urine,  for  very  many  of  the  same  ele- 
ments are  found  in  it  as  are  present  in  the  atrophied  stage 
of  the  inflammatory  form  and  in  the  cirrhotic  kidney, 
but  taken  in  connection  with  a  careful  study  of  the  his- 
tory of  the  case,  a  positive  diagnosis  can  generally  be 
reached. 

I  will  now  pass  to  the  consideration  of  the  causes  of  the 
cirrhotic  form  of  Bright' s  disease. 

ETIOLOGY. — The  two  most  common  causes  of  this  form 
of  kidney  degeneration  are  gout  and  rheumatism.  One  of 
these  causes  is  so  frequently  associated  with  its  develop- 
ment that  it  has  given  a  name  to  the  disease,  namely, 
"gouty  kidney." 

Cirrhotic  degeneration  of  the  kidneys,  when  associated 
either  with  rheumatism  or  gout,  is  probably  produced  by 
those  changes  in  the  blood  which  are  characteristic  of  a 
rheumatic  or  gouty  diathesis. 

The  constant  and  continued  use  of  alcohol  may  be  re- 
garded as  another  cause  of  cirrhotic  kidney,  for  we  not 
unfrequently  find  this  condition  of  the  kidney  associated 
with  cirrhosis  of  the  liver ;  and  the  same  steady  and  pro- 
longed indulgence  in  the  use  of  alcoholic  drinks  which 
produces  cirrhosis  of  the  liver,  may  produce  a  cirrhotic 
kidney.  These  three  are  the  principal  causes  of  cirrhotic 
kidney. 

This  condition  has  occasionally  been  met  with  in  connec- 
tion with  lead-poisoning,  therefore  lead-poisoning  has  been 
included  in  the  list  of  causes  of  cirrhotic  kidney. 

It  has  been  claimed  that  the  passive  congestion  of  the 
kidneys,  which  occurs  in  connection  with  some  forms  of 
heart  disease,  leads  to  the  development  of  cirrhotic  kidney. 


CIRRHOTIC   KIDNEY.  497 

I  have  already  shown  you  that  the  hardening  of  the  organs 
which  occurs  under  such  circumstances  is  due  to  changes 
in  the  blood-vessels  and  tubules,  rather  than  to  any  changes 
in  the  intertubular  tissue,  which  changes  are  almost  the 
reverse  of  those  which  occur  in  the  cirrhotic  kidney. 

SYMPTOMS. — The  symptoms  which  mark  the  develop- 
ment of  the  cirrhotic  form  of  Bright' s  disease,  are  even 
more  obscure  than  those  of  either  of  the  other  forms  of  the 
disease.  It  is  so  insidious  in  its  approach,  that  the  symp- 
toms which  mark  its  commencement  will  rarely  if  ever  be 
recognized.  One  of  the  earliest  and  most  constant  is  a 
frequent  desire  to  pass  urine.  There  may  be  no  albu- 
men nor  casts  in  the  urine,  no  dropsy,  and  none  of  the 
symptoms  which  usually  mark  the  presence  of  kidney 
disease. 

There  may  be  only  well-defined  nervous  symptoms  during 
life,  and  yet,  at  the  post-mortem  examination,  well-defined 
cirrhotic  kidneys  may  be  found. 

Usually  the  disease  is  developed  in  the  following  man- 
ner : 

An  individual  notices  that  he  is  growing  feeble  without 
any  apparent  cause  ;  he  is  suffering  from  dyspeptic  symp- 
toms ;  he  notices  that  he  is  passing  a  larger  quantity  of 
urine  than  normal,  and  perhaps  at  the  same  time  there  will 
be  a  slight  swelling  of  the  lower  extremities  after  prolonged 
exertion,  such  as  standing  or  walking.  This  oedema  comes 
and  goes,  is  more  marked  at  night  on  retiring,  disappearing 
in  the  morning  on  rising.  The  complexion  assumes  a  dingy 
hue.  • 

It  is  for  the  relief  of  their  dyspeptic  symptoms  this  class 
of  patients  usually  consult  their  physician,  and  a  plan  of 
treatment  is  adopted  for  their  relief,  with  the  assurance 
that  they  will  be  all  right  as  soon  as  they  can  leave  off  work 
and  take  a  rest.  A  single  examination  of  the  urine  may 
fail  to  detect  either  albumen  or  casts,  and  the  promises  of 
speedy  recovery  become  more  positive.  The  case  goes  on  ; 
the  patient  becomes  more  and  more  feeble,  he  has  a  care- 
worn look,  he  becomes  more  fretful  than  usual,  is  nervous 

and  restless,  and  finds  his  sleep  is  not  refreshing  ;  suddenly, 
32 


498  SYMPTOMS. 

when  under  excitement,  he  is  seized  with  convulsions, 
passes  into  coma,  remains  insensible  for  twenty-four  hours, 
and  dies. 

Perhaps  the  urine  was  examined  the  day  before  the  con- 
vulsion, and  no  albumen  was  found  ;  but  if  it  be  examined 
at  the  time  of  the  seizure,  both  albumen  and  casts  will  be 
found. 


LECTURE    XLII. 


BRIGHT' S    DISEASES. 

Cirrhotic  Kidney. — Symptoms,  etc. 

AT  my  last  lecture  I  gave  you  an  outline  history  of  the 
symptoms  which  attend  the  development  of  the  cirrhotic 
form  of  Bright' s  disease. 

This  morning  I  shall  consider  some  of  the  more  prominent 
of  these  symptoms  in  detail. 

There  are  in  this  form  of  Bright' s  disease,  as  in  the  other 
forms,  three  prominent  classes  of  symptoms,  namely,  the 
changes  in  the  urine,  the  dropsy,  and  the  nervous  phe- 
nomena. 

The  urine  is  increased  in  quantity,  and  of  low  specific 
gravity,  but  rarely  as  low  as  is  found  in  connection  with 
the  amyloid  kidney;  an  average  specific  gravity  in  this 
form  of  the  disease  is  1010.  It  is  characteristic  of  the  urine 
in  this  form  of  Bright' s  disease,  that  albumen  is  sometimes 
present  and  sometimes  absent.  We  do  not  know  why  this 
is  so.  In  the  other  forms  of  Bright' s  disease,  albumen  is 
always  found  in  greater  or  less  quantities  in  the  urine. 

When  the  urine  is  examined  for  casts,  it  may  be  necessary 
to  examine  several  specimens  before  casts  will  be  found,  but 
when  found,  they  usually  are  of  the  large  hyaline  variety. 
It  is  therefore  evident  that  a  positive  diagnosis  cannot 
always  be  arrived  at  by  a  single  examination  of  the  urine  ; 
several  examinations  are  frequently  necessary  before  any 
satisfactory  evidence  of  the  disease  can  be  obtained. 

It  is  just  here  that  mistakes  are  occasionally  made,  as . 


500  SYMPTOMS. 

this  class  of  patients  give  a  very  good  history  of  diabetes  ; 
they  suffer  from  thirst,  pass  a  large  quantity  of  urine,  have 
dyspeptic  symptoms,  and  present  marked  evidence  of  ema- 
ciation, and  when  the  urine  is  examined,  there  may  be 
neither  casts  nor  albumen  found.  But  the  application  of 
the  test  for  sugar  soon  settles  the  question ;  besides,  dia- 
betic urine  is  always  of  high  specific  gravity,  ranging  from 
1030  to  1040.  If  the  specific  gravity  of  the  urine  is  not 
more  than  1010,  the  case  may  be  regarded  as  one  of  the 
cirrhotic  form  of  Bright' s  disease. 

Dropsy  is  never  a  very  urgent  symptom  in  this  form  of 
kidney  disease.  Slight  oedema  of  the  feet  and  ankles  after 
exertion  is  present  in  almost  all  cases.  When  chronic 
oedema  of  the  feet  and  ankles  is  present,  and  is  associated 
with  the  general  symptoms  and  conditions  of  the  urine 
which  have  been  described,  you  need  not  hesitate  to  regard 
the  case  as  one  of  the  cirrhotic  form  of  Blight's  disease. 
General  anasarca  does  not  occur  in  this  form  of  the  disease. 
When  ascites  is  present,  it  is  due  to  changes  which  have 
taken  place  in  the  liver  rather  than  to  those  which  have 
taken  place  in  the  kidney. 

The  most  prominent  symptoms  connected  with  this  form 
of  Bright' s  disease  are  associated  with  the  nervous  system  ; 
the  explanation  of  this  clinical  fact  is  by  no  means  clear. 
These  symptoms  come  and  go  in  a  manner  not  readily 
understood.  The  earliest  and  most  constant  of  this  class  of 
symptoms  is  headache,  which  is  sometimes  most  violent  in 
character,  occurring  as  it  very  commonly  does  in  connection 
with  gout  and  rheumatism,  it  is  very  apt  to  be  regarded  as 
gouty  or  rheumatic  in  character.  With  these  headaches 
there  is  more  or  less  disturbance  of  nerve-function,  such  as 
vertigo,  temporary  inability  to  speak,  loss  of  sight  and 
hearing,  numbness,  neuralgic  pains,  cramps,  chorea,  tem- 
porary and  partial  paralysis  in  one  arm  or  leg.  There  may 
be  confusion  of  thought  or  impairment  of  memory  ;  con 
firmed  mania  may  be  developed.  These  patients  are  always 
liable  to  convulsions  after  unusally  severe  mental  or  physi- 
cal exertion  ;  from  the  convulsions  they  may  pass  into  a 
state  of  coma  ;  or  after  the  convulsions,  the  patient  may 


CIRKHOTIC   KIDNEY.  501 

become  drowsy,  with  more  or  less  delirium,  with  a  tongue 
brown  and  dry  ;  from  the  drowsiness  passing  into  a  state  of 
coma,  with  the  pupils  dilated.  In  both  cases  death  soon 
follows. 

It  is  probable  that  the  exciting  cause  of  this  disease  has 
very  much  to  do  with  the  development  of  these  nervous 
symptoms.  It  is  always  important  to  remember  the  dangers 
to  which  these  patients  are  constantly  exposed. 

In  some  cases  a  single  attack  of  violent  convulsions,  which 
has  been  preceded  by  intense  headache,  in  a  few  hours  ter- 
minates in  a  fatal  coma.  There  is  another  class  of  quite 
important  symptoms  which  attend  this  form  of  Bright' s 
disease,  regarded  by  some  as  complications.  The  most  con- 
stant of  these  is  cardiac  hypertrophy ;  it  is  present  to  a 
greater  or  less  degree  in  all  cases  of  contracted  kidney, 
when  the  disease  has  reached  an  advanced  stage.  In  some 
cases,  valvular  disease  or  atheromatous  and  calcareous 
degeneration  of  the  walls  of  the  large  arteries  is  sufficient  to 
explain  the  development  of  the  hypertrophy  ;  but  when  no 
such  obvious  causes  exist,  it  is  due  to  the  same  causes  as 
when  it  occurs  in  connection  with  the  atrophied  stage  of 
parenchymatous  nephritis. 

The  hypertrophy  in  such  cases  is  usually  confined  to  the 
left  ventricle.  The  presence  of  hypertrophy  of  the  left  ven- 
tricle without  any  assignable  cause,  such  as  valvular  disease, 
etc.,  is  sufficient  of  itself  to  direct  your  attention  towards 
the  kidneys  for  an  explanation  of  its  presence.  If  in  con- 
nection with  the  cardiac  hypertrophy,  the  urine  is  abundant 
and  of  low  specific  gravity,  containing  only  a  trace  of  albu- 
men, you  may  be  almost  certain  of  the  existence  of  this 
form  of  Bright' s  disease. 

Serous  inflammations  are  not  so  liable  to  occur  in  con 
nection  with  this  form  of  Bright' s  disease  as  in  connection 
with  the  inflammatory  form  ;  but  mucous  inflammations  are 
more  frequently  met  with  in  this  connection,  especially 
bronchitis,  which  assumes  a  chronic  type  and  alternates  with 
renal  and  gouty  symptoms. 

Amaurosis  is  one  of  the  most  serious  results  or  atten- 
dants of  a  cirrhotic  kidney.  In  the  early  stage  of  this 


bt£U  .-.  VI' 


502  DIFFERENTIAL   DIAGNOSIS. 

disease,  the  attacks  of  blindness  are  sudden  and  transient, 
and  are  of  ursemic  origin.  In  the  advanced  stages  of  this 
disease,  the  loss  of  sight  comes  on  gradually,  one  eye  only 
may  be  affected,  but  usually  both  eyes  are  equally  involved  ; 
the  cause  of  the  loss  of  sight  under  these  circumstances  is 
a  true  neuro-retinitis,  which  can  readily  be  recognized  by 
an  ophthalmoscopic  examination. 

In  the  advanced  stage  of  this  form  of  Bright' s  disease, 
hemorrhages  are  liable  to  occur  from  mucous  and  serous 
surfaces,  as  well  as  in  the  substance  of  organs.  The  cerebral 
is  the  most  serious  of  these  hemorrhages.  This  form  of 
renal  disease  is  more  frequently  associated  with  cerebral 
apoplexy  than  all  other  forms  ;  for,  with  this  form  you  are 
more  likely  to  have  degeneration  of  the  cerebral  arteries, 
and  the  increased  force  given  to  the  current  of  blood  by  the 
hypertrophied  left  ventricle  causes  rupture  of  the  weakened 
walls  of  the  cerebral  vessels. 

Interstitial  gastritis  is  frequently  met  with  in  connection 
with  this  form  of  renal  disease. 

DIFFERENTIAL  DIAGNOSIS. — I  have  but  few  words  to  say 
concerning  the  differential  diagnosis  of  this  form  of  Bright' s 
disease.  I  have  considered  it  in  connection  with  the  morbid 
anatomy  and  symptoms.  The  state  of  ursemic  stupor  to 
which  I  referred  in  the  history  of  its  symptoms,  when  the 
tongue  is  dry  and  other  typhoid  symptoms  are  present,  may 
be  mistaken  for  typhus  fever  ;  but  the  absence  of  the  char- 
acteristic eruption  of  the  fever,  and  the  quantity  and  com- 
position of  the  urine,  taken  in  connection  with  the  history 
of  the  case,  are  always  sufficient  for  a  diagnosis. 

The  presence  of  a  gouty  or  rheumatic  diathesis,  the 
insidious  development  of  the  disease,  the  large  quantity  of 
urine  secreted,  and  its  low  specific  gravity,  with  little  or  no 
albumen  present,  and  only  occasional  casts,  is  sufficient  to 
distinguish  this  form  of  Bright' s  disease  from  the  other 
forms  which  have  been  engaging  our  attention. 

PROGNOSIS. — The  prognosis,  as  far  as  regards  complete 
recovery,  is  bad.  When  the  anatomical  changes  which 
characterize  this  form  of  renal  disease  are  once  established, 
their  tendency  is  to  progress  ;  and  although  a  long  time  may 


CIERHOTIC   KIDNEY.  503 

elapse  from  their  commencement  to  the  fatal  termination, 
still  whenever  you  have  reason  to  believe  that  the  disease  is 
well  advanced,  you  must  remember  that  your  patient  is 
constantly  in  danger  from  the  complications  of  the  nervous 
system  to  which  I  have  referred. 

I  know  of  no  class  of  patients  who  are  surrounded  by  so 
many  forms  of  danger  as  those  suffering  from  advanced 
cirrhotic  degeneration  of  the  kidney. 

Before  passing  to  the  subject  of  the  treatment  of  the 
different  forms  of  Bright' s  disease  which  have  been  engag- 
ing our  attention,  I  will  briefly  review  some  of  the  more 
prominent  points  in  their  differential  diagnosis  and  prog- 
nosis. 

The  diagnosis  of  Bright' s  disease  can  always  be  made  if 
you  remember  the  clinical  history  and  the  changes  in  the 
urine  which  take  place  in  the  different  forms  of  renal  dis- 
ease which  I  have  been  describing.  A  positive  diagnosis  of 
any  one  of  these  forms  of  renal  disease  rests  upon  the 
presence  of  albumen  and  casts  in  the  urine.  The  presence 
of  albumen  alone  will  not  be  sufficient  evidence,  for  albu- 
men may  be  present  in  the  urine  under  a  variety  of  circum- 
stances where  no  organic  renal  disease  exists.  By  the 
exercise  of  proper  care,  the  failure  to  recognize  the  exist- 
ence of  any  form  of  Bright' s  disease  is  hardly  excusable. 

It  is  also  important  that  you  should  make  a  differential 
diagnosis  between  the  three  forms  of  disease  which  we  have 
been  considering,  for  upon  such  a  diagnosis  will  an  intelli- 
gent prognosis  and  treatment  very  much  depend. 

The  first  stage  of  tubular  inflammation  can  always  be 
recognized.  The  scanty  and  high-colored  urine,  the  large 
quantity  of  albumen,  and  the  presence  of  epithelial,  small 
hyaline,  and  blood-casts,  establish  the  existence  of  this 
stage  beyond  a  reasonable  doubt.  The  clinical  history  of 
this  form  is  also  entirely  different  from  that  of  either  of  the 
other  forms.  If  the  kidney  disease  has  followed  an  attack 
of  pneumonia,  scarlatina,  or  any  form  of  acute  disease,  or 
if  it  has  commenced  suddenly  (without  any  such  preceding 
history),  with  dropsy,  diminution  of  urine,  and  fever— or 
even  if  it  has  come  on  gradually,  with  dropsy  and  diminu- 


504  DIAGNOSIS. 

tion  of  urine,  you  may  be  almost  certain  that  your  case  is 
one  of  parenchymatous  nephritis. 

There  may  be  some  difficulty  in  distinguishing  by  the 
existing  symptoms  between  the  stage  of  atrophy  in  this 
form  and  advanced  amyloid  or  cirrhotic  degeneration  of  the 
kidney  ;  but  the  history  of  the  development  of  the  disease 
will  generally  enable  you  to  make  the  differential  diagnosis. 
The  one  is  an  inflammatory  affection  declared  by  great 
positiveness  of  symptoms  throughout  the  whole  course, — 
while  the  others  are  insidious  in  their  approach  and  are 
characterized  by  fluctuations  in  certain  of  their  symptoms. 

If  a  patient  with  evident  renal  disease  has  been  the  sub- 
ject of  syphilis,  chronic  suppuration,  or  some  exhausting 
disease,  and  his  illness  commences  insidiously  with  an 
abundant  urinary  secretion  containing  a  trace  of  albumen, 
amyloid  degeneration  of  the  kidney  is  indicated  ;  if  it  com- 
mences insidiously  with  no  positive  symptoms  until  an 
ursemic  convulsion  occurs,  or  dimness  of  vision  appears,  in 
one  who  is  the  subject  of  gout  or  rheumatism,  the  cirrhotic 
kidney  is  almost  certain  to  be  present. 

You  must  remember  that  inflammation  of  the  uriniferous 
tubes  may  be  engrafted  upon  either  the  amyloid  or  cirrhotic 
form  of  Bright' s  disease,  and  the  three  forms  of  disease 
may  be  united  in  the  same  kidney.  In  the  majority  of  in- 
stances, however,  a  careful  study  of  the  history  of  the 
patient,  and  repeated  chemical  and  microscopic  examina- 
tions of  the  urine,  will  enable  you  to  determine  whether 
the  disease  commenced  as  an  inflammation  of  the  urinifer- 
ous tubes,  or  as  an  amyloid  degeneration  of  the  blood- 
vessels of  the  kidneys,  or  as  a  cirrhotic  change  in  the  inter- 
tubular  structure. 

The  existence  of  waxy  liver  and  spleen  in  connection  with 
a  case  of  Bright' s  disease,  is  presumptive  evidence  of  the 
existence  of  waxy  kidney. 

The  existence  of  neuro-retinitis  is  also  strong  presump- 
tive evidence  of  a  cirrhotic  kidney. 

Hypertrophy  of  the  heart  is  met  with  in  the  advanced 
stages  of  all  forms  of  Bright' s  diseases,  but  especially  with 
the  cirrhotic  kidney. 


BEIGHT'S  DISEASES.  505 

The  prognosis  in  Bright' s  disease  varies  with  the  force 
and  stage  of  the  disease.  Recovery  is  always  possible  in 
the  first  stage  of  tubular  nephritis  ;  it  is  also  possible  in  the 
second  stage  ;  but  the  greater  proportion  of  recoveries  date 
from  the  first  rather  than  from  the  second  stage. 

^  Complete  recovery  is  never  possible  with  the  amyloid 
kidney,  with  the  cirrhotic  kidney,  or  in  the  atrophied  stage 
of  parenchymatous  nephritis.  In  each  of  these  conditions 
improvement  is  possible. 

In  the  first  stage  of  tubular  nephritis,  the  prognosis  will 
vary  with  the  character  and  intensity  of  the  inflammatory 
process.  Catarrhal  tubular  nephritis  may  be  completely 
recovered  from  in  nearly  every  instance.  When  the  inflam- 
matory process  is  croupous  in  character,  complete  recovery 
occurs  in  the  majority  of  instances ;  but  when  that  con- 
dition is  developed  in  which  degeneration  and  desquama- 
tion  of  the  epithelium  goes  on  slowly,  complete  recovery  is 
the  exception  to  the  rule.  When  the  stage  of  fatty  degen- 
eration is  reached,  the  prognosis  will  depend  very  much 
upon  the  character  of  the  first  stage  ;  if  the  fatty  stage  suc- 
ceeds a  catarrhal  or  croupous  inflammation,  the  proba- 
bilities are  that,  with  proper  management,  recovery  will 
take  place ;  if,  however,  the  fatty  stage  has  been  reached 
by  epithelial  degeneration,  and  there  are  evidences  of  ex- 
tensive obstruction  in  the  uriniferous  tubules,  the  chances 
for  complete  recovery  are  very  doubtful,  the  stage  of  gran- 
ular degeneration  and  atrophy  is  almost  certain  to  follow. 

The  length  of  time  required  for  a  patient  to  pass  through 
the  different  stages  of  this  form  of  Bright' s  disease  will  vary 
according  to  the  character  of  the  first  stage  ;  the  third  stage 
may  be  reached  within  six  or  eight  months  from  the  occur- 
rence of  the  earliest  symptoms. 

Amyloid  degeneration  of  the  kidneys  may  exist  for  many 
years,  and  yet  the  patient  enjoy  a  comparatively  good 
degree  of  health.  I  now  have  the  care  of  a  medical  gentle- 
man in  whom  the  disease  has  existed  certainly  eight  years, 
yet  he  is  in  such  good  health  as  to  be  able  to  discharge  the 
duties  incumbent  upon  a  large  country  practice. 

The  cirrhotic  form  of  kidney  is  also  slow  in  its  develop- 


506  DIAGNOSIS. 

ment,  and  patients  with  this  form  of  disease  may  live  many 
years  in  comparatively  good  health,  although,  as  I  have 
already  said,  they  are  constantly  in  danger  from  convulsions 
or  some  form  of  nervous  disturbance.  Therefore,  the  mere 
fact  that  albumen  and  casts  are  found  in  the  urine,  by  no 
means  positively  limits  the  life  of  the  patient. 

If,  however,  the  history  of  a  tubular  inflammation  pre- 
cedes or  accompanies  the  presence  of  albumen  and  casts  in 
the  urine,  with  the  evidences  that  the  tubular  inflammation 
has  reached  the  stage  of  atrophy,  the  prognosis  is  bad, 
both  as  regards  time  and  the  final  termination  of  the  case. 

Patients  with  this  form  of  Bright' s  disease  do  not  live  as 
long  as  those  who  are  the  subjects  of  either  of  the  other  forms 
of  the  disease.  The  most  favorable  prognosis,  short  of  com- 
plete recovery,  can  probably  be  given  in  connection  with  the 
amyloid  degeneration.  It  is  questionable  whether  amyloid 
degeneration  of  the  kidney  is  ever  an  immediate  cause  of 
death.  In  these  cases,  when  the  patients  die  with  renal 
symptoms,  death  is  produced  by  the  establishment  of  a 
tubular  inflammation  upon  the  waxy  change. 

You  will  notice  that  although  Bright' s  diseases  must 
always  be  regarded  as  grave  forms  of  disease,  yet  the  prog- 
nosis is  comparatively  good.  It  is  good  as  it  regards 
recovery,  in  the  first  and  second  stage  of  the  inflammatory 
form  ;  and  in  the  other  forms  of  the  disease,  as  far  as  dura- 
tion is  concerned,  the  cases  cannot  be  limited.  Their  dura- 
tion will  depend  upon  the  management  of  the  case  and  the 
circumstances  by  which  the  patient  is  surrounded,  rather 
than  upon  the  mere  fact  that  he  has  a  chronic  form  of 
kidney  disease. 

I  now  enter  upon  the  consideration  of  the  treatment  of 
the  different  forms  of  kidney  disease,  which  I  have  been 
describing  to  you  under  the  general  term  of  Bright' s 
diseases  of  the  kidney. 

TREATMENT. — This  is  the  most  interesting  and  at  the  same 
time  the  most  difficult  part  of  the  history  of  these  diseases. 
It  is  still  an  unsettled  subject ;  consequently,  in  discussing 
it,  1  shall  first  briefly  refer  to  some  of  the  principal  plans  oi 
treatment  which  have  been  resorted  to  for  their  cure,  and 


BEIGHT'S  DISEASES.  507 

afterward  speak  more  in  detail  of  those  means  which  I  have 
found  most  serviceable,  simply  giving  you  the  results  of  my 
own  experience. 

Formerly,  when  the  disease  was  regarded  as  an  albumi- 
nous nephritis,  general  and  local  blood-letting  was  practised  ; 
this  was  soon  found  to  be  attended  with  bad  results.  At 
the  present  time,  general  blood-letting  is  never  resorted  to, 
unless  it  be  in  that  very  acute  form  of  parenchymatous 
nephritis  which  is  attended  by  violent  cerebral  symptoms. 
There  are  some  who  believe  that  general  bleeding  is  service- 
able -under  such  circumstances,  but  it  is  not  practised  in 
any  other  form  of  the  disease. 

At  one  time,  mercurials  were  extensively  employed  in  the 
treatment  of  these  diseases,  with  the  idea  of  putting  the  sys- 
tem under 'its  constitutional  effects  and  keeping  it  so  for 
months.  This  plan  has  also  been  abandoned  ;  there  are 
some,  however,  who  claim  that  in  the  form  of  the  bichloride 
it  can  be  employed  with  benefit.  I  shall  hereafter  name  to 
you  a  class  of  cases  in  which  the  administration  of  this 
form  of  mercury  is  admissible.  Mercury,  however,  should 
not  be  employed  as  a  remedy  for  general  use  in  the  treat- 
ment of  these  diseases,  simply  because  a  very  limited  class 
of  cases  are  benefited  by  its  administration. 

Ptyalism  is  not  admissible  in  any  form  of  the  disease. 

As  soon  as  the  pathology  of  the  disease  became  better 
understood,  an  entirely  different  plan  of  treatment  was 
adopted,  based  upon  entirely  different  principles.  The 
kidneys  came  to  be  regarded  as  the  seat  of  an  inflammation, 
and  the  proposition  was,  that  the  first  essential  in  the  treat- 
ment of  an  inflamed  organ  was  rest.  It  was  proposed  to 
treat  Bright' s  disease  upon  the  same  principle  as  an  inflamed 
eye  or  inflamed  joint  would  be  treated  ;  that  is,  give  the 
kidneys  perfect  rest. 

Under  this  plan  of  treatment,  there  was  no  distinction 
made  with  regard  to  the  different  forms  of  the  disease. 

The  principle  of  giving  rest  to  an  inflamed  organ,  is  a 
very  important  one  under  certain  conditions,  but  the  con- 
dition of  affairs  with  an  inflamed  eye,  or  an  inflamed  joint, 


508  TKEATMENT. 

is  very  different  from  that  which  is  presented  by  the  kid- 
neys in  the  different  forms  of  Bright' s  disease. 

Carrying  out  this  idea,  it  was  proposed  to  supplant  the 
function  of  the  kidneys  as  far  as  possible  by  increasing  the 
function  of  the  skin ;  that  is,  the  skin  was  to  perform  the 
work  of  the  kidneys.  Upon  this  principle  was  based  what 
is  known  as  the  diaplioretic  plan  of  treatment.  Very  soon, 
a  strong  addition  was  made  to  the  diaphoretic  plan,  by 
calling  in  the  assistance  of  hydragogue  cathartics.  The 
principle  of  these  two  plans  of  treatment  was  to  eliminate 
the  urea  by  means  of  remedies  addressed  to  the  skin  and 
the  mucous  membrane  of  the  intestines,  and  allow  the  in- 
flamed kidneys  to  rest. 


LECTURE    XLIII. 


BBIGHT'S  DISEASES. 

Treatment.     (  Continued. ) 

AT  the  close  of  my  last  lecture  I  was  speaking  to  you  of 
the  diaphoretic  plan  of  treatment  in  Bright' s  disease  of  the 
kidneys.  I  will  continue  the  subject  this  morning,  by 
describing  the  manner  in  which  this  plan  of  treatment  is 
practised. 

The  patient  should  be  placed  in  bed,  covered  with  flannel 
blankets,  and  by  means  of  an  apparatus  procured  of  any 
instrument-maker,  hot  air  should  be  constantly  introduced 
beneath  the  bed-clothes,  and  thus  profuse  perspiration  will 
be  induced,  and  the  excretory  power  of  the  skin  taxed  to 
its  utmost. 

The  bath  should  be  continued  from  half  an  hour  to  an 
hour,  or  even  longer  ;  then  the  patient  should  be  allowed  to 
gradually  become  cool,  and  when  so,  to  resume  his  clothing 
and  walk  about  the  room  or  ward,  the  temperature  of  which 
should  be  above  70°  F.  These  baths  may  be  repeated  once 
or  twice  each  day,  or  every  other  day,  as  the  condition  of 
the  patient  may  demand. 

When  I  entered  the  profession,  the  diaphoretic  was  the 
leading  plan  of  treatment. 

The  effect  usually  produced  by  the  employment  of  this 
plan  of  treatment  is  a  rapid  subsidence  of  the  oedema.  It 
may  not  require  more  than  half  a  dozen  hot-air  baths  to 
entirely  remove  the  dropsy  from  a  "water-logged"  patient, 
and  as  far  as  that  one  symptom  is  concerned,  to  give  com- 


610  TREATMENT. 

plete  relief,  but  the  relief  is  only  temporary.  Soon  the 
patient  becomes  anaemic,  loses  his  strength,  and  as  the  pro- 
cess goes  on,  a  point  is  reached  at  which  the  oedema  re- 
turns, although  the  hot-air  baths  are  continued,  and  the 
effects  of  urea  upon  the  general  system  become  more  marked. 
I  have  seen  patients  pass  into  convulsions  while  the  hot-air 
baths  were  being  used.  Under  such  circumstances,  it  is 
customary  to  administer  hydragogue  cathartics  in  suf- 
ficiently large  doses  to  produce  daily  three  or  four  watery 
discharges  from  the  bowels.  It  is  true  that  under  the  con- 
joined action  of  these  two  plans,  this  class  of  patients  for  a 
time  will  appear  very  much  relieved  ;  but  after  a  few  active 
purgations,  and  a  few  hot-air  baths,  they  will  begin  to 
complain  of  extreme  weakness,  and  very  soon  reach  a  point 
at  which  the  combined  action  of  these  agents  fails  even  to 
relieve  the  distressing  symptoms,  and  their  condition  is 
worse  than  before  their  administration  was  commenced. 

Several  years  ago  I  became  convinced  that  this  depurative 
plan  of  treatment  was  wrong,  and  that  it  was  wrong  be- 
cause it  rapidly  depleted  patients  that  could  not  bear 
depletion.  Exhaustion  can  as  certainly  be  produced  by 
profuse  diaphoresis  and  hydragogue  cathartics,  as  by  re- 
peated general  bleedings,  and  urea  may  as  well  be  elimi- 
nated by  drawing  blood  from  the  arm  as  by  hydragogue 
cathartics  and  diaphoretics.  Besides,  the  repeated  use  of 
hydragogue  cathartics  interferes  with  the  processes  of  di- 
gestion and  assimilation.  I  wrould  not  discard  these  reme- 
dies, but  hold  them  in  reserve.  They  do  not  enter  promi- 
nently into  my  plan  of  treatment. 

In  the  first  stage  of  parenchymatous  nephritis,  there  are 
three  important  things  to  be  accomplished  by  treatment. 

First :  The  elimination  of  urea. 

Second :  The  removal,  as  rapidly  as  possible,  of  the  in- 
flammatory products  which  obstruct  the  uriniferous  tu- 
bules. 

TJiird:  To  counteract  the  effect  of  urea  upon  the  ner- 
vous system. 

The  question  arises,  how  shall  we  meet  these  indications  ? 

The  first  thins  to  be  done  is  to  remove  the  exudation 


BRIGHT' s  DISEASES.  511 

which  obstructs  the  uriniferous  tubules.  This  exudation 
not  only  stops  the  elimination  of  urea,  by  preventing  the 
kidneys  from  performing  their  normal  eliminative  function, 
but  if  it  remains  in  the  tubules  it  develops  a  degenerative 
inflammation. 

In  treating  a  case  of  bronchitis,  you  would  not  favor  an 
accumulation  in  the  bronchi  by  preventing  expectoration, 
but  you  would  aid,  in  all  possible  ways,  free  and  un- 
obstructed expectoration. 

The  same  condition  of  affairs  obtains  in  the  first  stage  of 
parenchymatous  nephritis ;  the  inflammatory  products  so 
obstruct  the  uriniferous  tubules  as  to  prevent  these  organs 
from  performing  their  proper  functions. 

If  the  secretive  power  of  the  kidneys  can  be  so  increased 
that  they  will  pour  out  fluid  in  sufficient  quantity  to  carry 
off  this  material,  a  result  will  have  been  accomplished  of 
great  importance  in  the  management  of  this  class  of  cases. 
Digitalis  is  the  remedy  I  would  recommend  for  the  accom- 
plishment of  such  a  result,  as  it  increases  the  urinary  secre- 
tion without  stimulating  the  kidneys,  to  which  there  is  so 
much  objection.  I  am  convinced  that  it  does  not  act  as  a 
diuretic  by  stimulating  the  kidneys  ;  but  by  increasing  the 
power  of  the  heart' s  action,  it  overcomes  the  obstruction  in 
the  renal  circulation,  and  thus  causes  an  increased  flow  of  the 
watery  portion  of  the  urine  through  the  Malpigliian  tufts 
into  the  upper  portion  of  the  uriniferous  tubules.  Thus  the 
obstruction  in  the  tubes  is  washed  out,  and  at  the  same 
time  you  have  called  into  action  the  eliminative  functions 
of  the  kidneys,  so  that  the  urea  is  carried  out  of  the  system 
much  more  rapidly  and  completely  than  it  can  be  by  the 
skin  or  bowels.  By  the  action  of  digitalis,  we  really 
diminish  the  quantity  of  blood  in  kidneys  that  are  the  seat 
of  inflammatory  congestion. 

The  statements  made  under  the  head  of  acute  ursemia,  in 
regard  to  the  use  and  effects  of  digitalis,  are  true  in  this  con- 
nection. 

If  any  benefit  is  to  be  derived  from  this  drug,  in  the  first 
stage  of  parenchymatous  nephritis,  it  must  be  administered 
in  large  doses.  In  this  stage,  I  usually  administer  half  an 


512  TKEATMENT. 

ounce  of  the  infusion  every  two  hours  for  twenty-four 
hours,  and  then  wait  twelve  hours  and  watch  its  effects ; 
after  which,  I  continue  its  administration  in  smaller  doses 
and  at  longer  intervals,  so  long  as  the  uraemic  symptoms 
are  urgent. 

In  connection  with  the  administration  of  digitalis,  I 
would  recommend  the  application  of  dry  cups  over  the 
region  of  the  kidneys.  In  order  that  the  dry  cupping  may 
be  more  effectual,  each  cup  should  be  removed  as  soon  as 
the  vessels  beneath  are  well  filled.  The  object  is,  first,  to 
draw  the  blood  from  the  arteries  into  the  capillaries,  not 
with  sufficient  force  to  cause  extravasation,  the  effect  of 
which  would  be  to  impede  the  circulation  through  vessels  of 
the  skin,  and  so  cause  more  blood  to  be  driven  into  the  in- 
flamed tissue  underneath.  The  object  of  dry  cupping  is  not 
to  irritate  the  surface,  but  to  rapidly  draw  the  blood  from 
the  arteries  and  as  rapidly  carry  it  through  the  capillaries 
to  the  veins  in  the  backward  course  to  the  heart.  After  dry 
cupping,  warm  poultices  over  the  kidneys  may  be  applied 
with  benefit ;  digitalis  leaves  may  be  used  for  a  poultice, 
and  thus  applied,  they  will  increase  the  diuretic  effect  of 
the  drug  which  has  already  been  administered  internally. 
After  the  free  administration  of  digitalis  and  the  applica- 
tion of  dry  cups  to  the  kidneys,  if  the  ursemic  symptoms 
are  still  urgent,  hot-air  baths  and  hydragogue  cathartics 
may  temporarily  be  resorted  to,  to  aid  in  carrying  the 
patient  over  the  period  of  greatest  danger,  but  their  use 
should  not  be  continued  after  free  diuresis  is  established. 

In  the  management  of  the  first  stage  of  parenchymatous 
nephritis,  these  are  the  principal  means  to  be  made  use  of. 
The  next  object  to  be  accomplished  is  the  relief  of  the 
nervous  system  from  the  poisonous  effects  of  the  excess  of 
urea.  In  the  first  stage  of  this  form  of  Bright' s  disease,  a 
large  amount  of  urea  may  rapidly  accumulate  in  the  circu- 
lation, causing  intense  headache,  restlessness,  and  perhaps 
convulsions  and  coma.  Under  these  circumstances,  the 
means  to  be  employed  are  the  same  as  in  the  treatment  of 
acute  uraemia. 

I  will  not  now  detain  you  with  their  enumeration,  as  I 


BEIGHT'S  DISEASES.  513 

have  already  mentioned  them  in  my  lecture  upon  acute 
uraemia.  It  is  important  that  the  diuretic  plan  of  treat- 
ment should  be  continued  after  the  patient  has  passed  into 
the  second  stage.  The  administration  of  the  digitalis 
should  be  continued  in  moderate  doses.  Having  passed  the 
first  danger,  a  second  danger  arises,  namely,  that  the  fatty 
stage  will  pass  on  to  the  stage  of  atrophy.  It  is  important 
that  the  fatty  accumulations  should  be  removed  as  rapidly 
as  possible  from  the  uriniferous  tubules.  The  more  abun- 
dant the  urinary  flow,  the  more  completely  will  the  urinifer- 
ous tubules  be  washed  out. 

There  is  another  element  which  enters  into  the  treatment 
in  this  stage  of  the  disease, — the  establishment  of  healthy 
nutrition  in  the  kidneys.  In  parenchymatous  nephritis, 
nutrition  of  the  kidneys  is  always  imperfectly  performed, 
and  patients  are  more  or  less  anaemic.  For  this  reason  it  is 
important  that  the  nutritive  processes  be  carried  to  their 
highest  point ;  that  as  the  obstructions  are  removed  from 
the  uriniferous  tubes,  the  degenerative  inflammatory  pro- 
cesses may  be  arrested  and  the  epithelial  lining  of  the  tubes 
restored.  In  the  second  stage  of  this  disease,  you  will  there- 
fore administer  digitalis  in  sufficient  quantity  to  produce 
moderate  diuresis,  and  at  the  same  time  iron  should  be 
given  with  a  most  nutritious  diet.  If  milk  does  not  dis- 
agree with  the  patient,  it  will  be  found  the  best  article  of 
diet ;  it  may  be  taken  cold  or  hot,  from  a  half  pint  to  a  pint 
at  a  time.  Adults  will  often  take  three  or  four  quarts  in 
twenty -four  hours.  Milk  is  readily  digested,  and  when 
taken  freely,  supplies  an  abundance  of  liquid,  which  acts 
to  a  certain  extent  as  a  diuretic.  In  some  cases  a  moderate 
amount  of  stimulants  will  be  beneficial.  Wines  are  to  be 
preferred,  and  they  must  be  taken  with  the  food.  The 
patient  must  be  surrounded  by  the  best  hygienic  influences, 
be  kept  in  a  uniform  temperature  in  well- ventilated  apart- 
ments, and  the  surface  of  the  body  must  be  covered  with 
flannel.  The  secretion  of  urine  must  be  carefully  observed 
both  as  to  its  quantity  and  quality.  In  this  stage,  if  the 
patient  recovers,  the  recovery  must  commence  before  a 

33 


514  TKEATMEISTT. 

tubular  degenerative  process  commences,  and  the  indica- 
tions of  recovery  will  show  themselves  within  six  weeks 
after  its  commencement. 

In  the  stage  of  atrophy,  there  will  be  no  necessity  for  the* 
administration  of  diuretics.     This  stage  is  marked  by  an 
abundant  flow  of  urine  of  low  specific  gravity. 

This  increase  in  the  quantity  of  the  urine  is  marked  by 
great  feebleness  of  the  vital  powers,  consequently  a  support- 
ing plan  of  treatment  is  indicated.  Usually  this  class  of 
patients,  on  account  of  their  feeble  digestive  power,  will  be 
compelled  to  take  food  in  small  quantities  and  at  short 
intervals,  and  they  will  be  greatly  benefited  by  the  daily 
use  of  cod-liver  oil  and  iron.  Wines  taken  in  moderation 
with  the  food  often  are  of  service. 

Great  care  should  be  taken  that  the  surface  of  the  body 
is  not  exposed  to  sudden  changes  of  temperature,  and,  if 
possible,  such  patients  should  take  up  their  residence  in  a 
warm  climate. 

Whenever  the  urine  is  scanty,  two  or  three  full  doses  of 
digitalis  should  be  administered,  for  there  is  danger  that  an 
acute  tubular  inflammation  may  be  developed,  and  it  is 
very  important  that  the  earliest  development  of  those  S37mp- 
torns  which  indicate  a  tendency  in  that  direction  should  be 
met  by  the  application  of  dry  cups  over  the  kidneys,  and 
the  free  administration  of  digitalis. 

Let  me  now  briefly  recapitulate  the  principal  things  to  be 
observed  in  the  management  of  this  form  of  Bright' s 
disease. 

In  the  acute  stage,  whatever  may  have  been  the  exciting 
cause,  the  patient  must  be  kept  in  bed,  in  a  large,  well- 
ventilated  apartment,  with  a  temperature  of  75°  F. ;  milk 
should  be  his  only  article  of  diet.  Dry  cups  should  be 
applied  over  the  kidneys,  and  the  infusion  of  digitalis 
should  be  freely  administered. 

If  this  plan  is  systematically  carried  out  at  the  very 
commencement  of  this  stage,  the  urine  soon  becomes 
copious,  the  albumen  in  the  urine  gradually  diminishes, 
and  the  dropsy  passes  away.  As  soon  as  the  flow  of 
urine  commences,  the  administration  of  digitalis  must  be 


BKIGHT'S  DISEASES.  515 

discontinued,  and  diluent  drinks  freely  administered  to 
keep  up  the  diuresis.  If  renal  secretion  is  not  restored 
within  twenty -four  hours  after  the  commencement  of  this 
plan  of  treatment,  in  addition,  warm  baths  or  hot-air  baths 
must  be  used  ;  and  if  the  symptoms  are  urgent,  hydragogue 
cathartics  may  be  administered.  If  convulsions  or  coma 
threaten,  morphine  must  be  administered  hypodermically 
in  sufficiently  large  doses  to  control  the  nervous  disturb- 
ance. 

If  the  patient  has  reached  the  second  or  third  stage  of 
the  disease,  a  condition  commonly  called  chronic  Bright' s 
disease,  the  urgent  symptoms,  such  as  dropsy,  etc.,  must 
be  relieved  by  an  occasional  hot-air  bath,  hydragogue 
cathartics  or  stimulating  diuretics,  and  at  the  same  time 
great  care  must  be  exercised  lest  the  depletion  be  carried 
too  far. 

Iron  and  cod-liver  oil  are  the  two  great  remedial  agents  in 
this  stage  of  the  disease,  and  should  be  daily  administered, 
unless  the  condition  of  the  stomach  of  the  patient  shall  con- 
tra-indicate  their  use.  Milk  should  be  the  principal  article 
of  diet. 

By  living  in  a  warm  climate,  by  constant  watchfulness, 
and  by  following  the  rules  I  have  given,  a  fatal  termination 
may  be  long  delayed,  although  complete  recovery  can  hardly 
be  hoped  for  in  this  form  of  Bright' s  disease. 

Let  me  impress  upon  your  mind  this  fact :  that  no  deplet- 
ing remedies  should  be  employed  in  the  second  and  third 
stage  of  this  form  of  Blight's  disease,  except  in  times  of 
emergency,  when  from  some  sudden  renal  congestion  the 
function  of  that  portion  of  the  kidney-structure  which  is 
still  performing  the  work  of  elimination,  shall  suddenly  be 
arrested  or  impaired,  and  active  ursemic  symptoms  shall  be 
developed. 

The  plan  of  treatment  in  this  stage  is  essentially  tonic. 

I  will  now  briefly  consider  the  treatment  of  amyloid 
degeneration  of  the  kidney. 

So  far  as  I  am  aware,  this  is  an  incurable  disease  ;  we  have 
no  means  for  arresting  or  preventing  its  development.  It  is 
rarely  the  case  that  any  one  organ  is  alone  affected  by  this 


516  TREATMENT. 

form  of  degeneration.  The  same  general  principles  are  to 
govern  ns  in  the  treatment  of  amyloid  degeneration  of  the 
kidney  as  govern  us  in  the  treatment  of  waxy  degeneration 
in  any  other  organ  of  the  body.  First,  if  possible,  remove 
its  cause.  If  it  occurs  in  connection  with  disease  of  the 
bones,  or  any  prolonged  suppuration,  the  diseased  bone 
must  be  removed,  and  the  purulent  accumulations  must  be 
removed  or  prevented.  If  it  depend  upon  syphilis,  you 
will  at  once  make  use  of  anti-syphilitic  remedies,  always 
remembering  that  waxy  degeneration  occurs  only  in  con- 
nection with  the  tertiary  manifestations  of  syphilis,  and 
that  all  measures  which  have  a  tendency  to  debilitate  the 
patient  must  be  avoided.  Iodide  of  potassium  and  mer- 
cury are  the  most  prominent  remedial  agents  in  this  stage 
of  syphilis.  Both  of  these  agents  have  gained  some  favor  as 
remedies  in  the  treatment  of  Bright' s  disease,  and  there  are 
those  who  employ  indiscriminately  one  or  the  other  or  both  of 
them.  The  benefit  derived  in  certain  cases  from  their  use,  is 
undoubtedly  due  to  their  power  over  syphilitic  manifesta- 
tions. In  such  cases,  the  long-continued  use  of  small  doses  of 
mercurials  will  generally  be  followed  by  marked  improve- 
ment, but  care  should  be  exercised  that  their  use  is  not  con- 
tinued until  the  specific  effect  of  the  drug  is  produced  upon 
the  system.  When  these  patients  are  in  a  debilitated  con- 
dition, it  is  not  well  to  administer  mercury.  Iodide  of 
potassium  will  be  of  greater  service  when  in  connection  with 
it  cod-liver  oil  and  other  tonics  are  used. 

The  form  of  iodine  which  I  have  found  most  serviceable 
in  the  treatment  of  this  class  of  patients  is  Blancard's  pills. 
One  of  these  pills  given  three  times  a  day,  at  the  time  of 
taking  food,  will  be  followed  by  the  most  beneficial  results. 

Diuretics  and  hydragogue  cathartics  will  rarely  be  re- 
quired in  the  treatment  of  this  form  of  Bright' s  disease. 

When  the  inflammatory  form  becomes  engrafted  upon 
the  amyloid,  the  administration  of  diuretics  and  hydra- 
gogue cathartics  may  be  temporarily  required,  and  dry 
cups  to  the  lumbar  region  will  be  of  service. 

The  symptoms  of  the  inflammatory  form  of  this  disease 
are  similar  to  those  which  are  manifested  when  it  is  devel- 


BRIGHT' s  DISEASES.  517 

oped  under  other  circumstances  ;  they  will  therefore  be 
treated  upon  the  same  general  principles,  and  according  to 
the  rules  which  have  already  been  given  for  its  manage- 
ment. 

The  cirrhotic  form  of  Bright' s  disease  is  the  most  hope- 
less of  all  the  forms  of  this  disease.  When  cirrhosis  of 
the  kidney  is  once  developed,  its  tendency  is  to  progress  ; 
more  and  more  of  the  interstitial  tissue  of  the  organ  becomes 
involved  ;  the  tubules  become  more  and  more  obliterated,  as 
a  result  of  the  gradual  diminution  in  the  eliminating  power 
of  the  kidneys  ;  the  dangers  which  attend  these  patients 
steadily  increase,  and  the  disturbance  of  the  nervous  func- 
tions becomes  more  and  more  marked. 

In  this  form  of  the  disease  little  is  to  be  gained  by  the 
adoption  of  any  special  plan  of  treatment. 

It  has  been  claimed  that  the  long-continued  administra- 
tion of  mercury  in  small  doses  has  the  power  to  arrest  or 
prevent  connective-tissue  development,  but  there  is  no  posi- 
tive evidence  that  it  has  any  such  power  ;  besides,  in  most 
instances,  cirrhotic  kidney  is  developed  in  connection  with  a 
gouty  or  rheumatic  diathesis,  which  most  positively  con- 
tra-indicates  the  use  of  mercurials.  When  this  form  of 
kidney  is  developed  in  connection  with  lead-poisoning, 
mercurials  are  most  decidedly  contra-indicated.  Mercu- 
rials can  be  employed  with  possible  advantage  only  in 
those  cases  in  which  cirrhotic  kidney  is  developed  in  con- 
nection with  cirrhosis  of  the  liver.  Bichloride  of  mercury  is 
the  preparation  usually  employed. 

If  the  disease  occurs  in  connection  with  gout  or  rheuma- 
tism, the  same  class  of  remedies  which  are  employed  to 
relieve  gouty  or  rheumatic  manifestations,  will  give  relief 
to  the  kidney  complications.  , 

In  other  words,  when  this  class  of  patients  suifer  from 
headache,  and  become  restless,  nervous,  and  tremulous, 
they  will  be  benefited  by  the  same  class  of  remedies  that 
give  relief  when  they  are  suffering  from  an  attack  of  gout 
or  rheumatism.  Many  of  these  patients  will  derive  great 
benefit  from  residing  for  a  time  in  those  localities  where 
they  may  constantly  use  water  from  alkaline  springs.  I 


518  TREATMENT. 

f 

have  known  very  many  persons  with  a  gouty  or  rheumatic 
diathesis,  markedly  relieved  of  their  articular  gouty  man- 
ifestations, as  well  as  of  their  kidney  complications,  by  a 
residence  at  Richfield  Springs  in  this  State,  or  at  the  Vir- 
ginia Springs. 

The  Germans  have  made  much  more  extended  observations 
than  we,  in  regard  to  alkaline  waters  and  their  systematic 
use  in  the  treatment  of  this  class  of  diseases. 

Iron  is  not  as  serviceable  in  the  treatment  of  this  form  of 
Bright' s  disease  as  in  the  treatment  of  patients  with  amy- 
loid kidney,  or  those  in  the  stage  of  atrophy  or  parenchy- 
matous  nephritis.  Although  these  patients  appear  anaemic, 
their  nervous  symptoms  are  aggravated  rather  than  relieved 
by  the  use  of  iron.  I  have  found  strychnine  a  much  more 
serviceable  remedy.  It  should  be  administered  in  minute 
doses  for  a  very  long  time.  In  a  certain  proportion  of  cases, 
cod-liver  oil  will  be  found  of  service,  especially  when  com- 
bined with  the  hypophosphate  of  soda. 

As  a  rule,  diuretics  are  not  of  service. 

In  those  cases  where  a  marked  diminution  in  the  urinary 
secretion  occurs,  their  temporary  employment  to  aid  in 
restoring  this  function  may  be  of  service.  When  the  dis- 
ease is  developed  in  connection  with  cirrhosis  of  the  liver, 
the  use  of  hydragogue  cathartics  may  be  attended  with 
benefit. 

It  is  of  the  utmost  importance  that  this  class  of  patients 
should  make  a  permanent  residence  in  a  warm  climate,  and 
that  all  the  exciting  causes  of  cirrhotic  development  should 
be  carefully  avoided.  Although  you  may  not  hope  to  cure 
the  disease,  you  may  hope  to  delay  its  progressive  develop- 
ment, and  by  carefully  watching  the  condition  of  the  ner- 
vous system,  and  by  timely  interference,  delay  or  prevent  the 
development  of  the  graver  forms  of  nervous  disturbance, 
and  so  prolong  the  life  of  your  patient. 

For  the  successful  management  of  all  forms  of  Bright' s 
disease,  permanent  residence  in  a  warm  climate,  and  a  care- 
ful observance  of  all  the  rules  of  hygiene,  is  necessary. 

In  advanced  cases,  whenever  there  is  extensive  general 
anasarca,  and  the  respiration  becomes  impeded  by  the  ac- 


BRIGHT  S   DISEASES.  619 

cumulation  of  fluid  within  the  chest-walls,  or  by  an  oede- 
matous  condition  of  the  lungs,  and  all  other  means  have 
failed  to  relieve  the  dropsy,  prompt  and  sometimes  per- 
manent relief  may  be  afforded  by  making  free  incision 
through  the  skin  into  the  areolar  tissue  above  the  ankles. 

Those  dyspeptic  and  gastric  symptoms  which  are  so  ob- 
stinate and  distressing  in  the  chronic  stages  of  these  diseases, 
usually  can  only  be  relieved  by  a  carefully  regulated  diet. 

The  principles  which  are  to  govern  you  in  the  manage- 
ment of  the  great  variety  of  unpleasant  and  dangerous 
manifestations  and  complications  that  occur  in  the  different 
forms  and  stages  of  Bright' s  diseases  which  we  have  been 
studying,  have  already  been  sufficiently  considered.  I  shall 
not  detain  you  with  their  further  consideration. 

In  these  lectures  I  have  endeavored  to  give  you  an  out 
line  history  of  the  different  forms  of  Bright' s  diseases  of  the 
kidney,  and  to  fix  in  your  mind  the  prominent  points  in 
their  history. 


LECTURE    XLIV. 


PYELITIS. 

Pyonephrosis. — Hydronephrosis. — Cystic  Kidney. — Renal  Concretions. — 
Growths  in  the  Kidney. 

THIS  morning  I  will  invite  your  attention  to  a  disease  of 
the  kidneys,  named  pyelitis,  which  bears  a  close  connection 
to  those  diseases  of  the  kidneys  which  have  so  recently 
been  under  consideration.  It  is  an  inflammation  of  the 
mucous  membrane  of  the  pelvis  and  calices  of  the  kidney, 
and  may  run  an  acute  or  chronic  course.  It  may  involve 
the  pelvis  and  infundibula  of  one  kidney,  or  both  kidneys 
may  be  the  seat  of  disease. 

MOKBID  ATST ATOMY. — As  regards  the  morbid  changes 
which  take  place  in  a  case  of  acute  pyelitis,  you  wili  first 
notice  that  the  mucous  membrane  of  the  pelvis  of  the 
kidney  is  more  or  less  congested.  When  very  much  con- 
gested, the  surface  will  be  dotted  here  and  there  with  little 
dark-red  spots  which  are  minute  ecchymoses.  You  will  also 
notice  that  the  epithelial  covering  of  the  mucous  membrane 
is  more  or  less  removed  ;  at  one  time  it  is  entirely  removed, 
at  another  time  it  is  removed  in  patches.  As  the  congestion 
increases,  more  or  less  muco-purulent  secretion  may  be  found 
covering  the  surface  of  the  mucous  membrane  and  more  or 
less  completely  filling  the  cavity.  In  the  acute  stage,  the 
purulent  secretion  is  comparatively  slight. 

In  a  certain  class  of  cases,  a  membranous  exudation  may 
be  developed  upon  the  mucous  membrane  of  the  pelvis  of 
the  kidney.  It  is  a  diphtheritic  exudation  occurring  in  con- 
nection with  diphtheritic  exudations  in  other  parts  of  the 
body,  then  it  becomes  a  complication  of  general  diphtheria, 


PYELITIS.  521 

and  is  called  diphtheritic  pyelitis.  This  diphtheritic  mem- 
branous exudation  is  liable  to  become  detached  and  block 
up  the  ureter. 

This  affection  may  occur  as  a  catarrhal  inflammation,  or 
the  inflammation  may  be  of  a  croupous  nature.  The 
croupous  variety  is  rare. 

In  chronic  pyelitis,  the  mucous  membrane  of  the  pelvis 
of  the  kidney  is  not  only  very  much  thickened,  but  it 
undergoes  a  change  of  color.  It  becomes  of  a  grayish- 
white  or  slate-color,  and  is  traversed  by  dilated  veins.  It  is 
thickened,  and  the  pelvis  and  infundibula  are  dilated. 
Pus  is  more  or  less  abundantly  formed,  and  if  there  is  no 
obstruction,  it  flows  away  with  the  urine.  Should  there  be 
an  impediment  to  its  escape  it  accumulates  in  the  pelvis, 
which  it  distends  more  and  more,  and  at  last  gives  rise  to  a 
condition  known  as  pyonephrosis.  This  dilatation  as  it 
progresses  encroaches  first  on  the  papillae  which  become  flat- 
ened  and  obliterated,  next  on  the  pyramids,  and  finally,  by 
the  pressure  it  causes,  the  cortical  portion  of  the  kidney 
disappears.  In  such  cases  you  may  have  remaining  only  a 
sacculated  pouch  containing  from  an  ounce  to  several 
ounces  of  fluid,  which  may  be  composed  of  pus,  broken- 
down  material,  and  more  or  less  calcareous  matter.  Not 
only  will  you  have  these  changes  taking  place  in  the  mu- 
cous lining  of  the  pelvis,  but,  if  there  is  a  renal  calculus 
present,  which  is  the  cause  of  the  pyelitis,  more  or  less  ex- 
tensive ulceration  of  the  mucous  membrane  may  be  estab- 
lished. These  ulcerations  may  extend  beyond  the  normal 
limits  of  the  membrane,  cause  perforation  of  the  pelvis,  and 
give  rise  to  extravasation  of  urine  into  the  adjacent  tissue. 

Again,  you  may  have  the  ureters  of  the  kidney,  which  is 
the  seat  of  the  pyelitis,  completely  or  partially  obstructed, 
and  pus,  blood  and  urinous  material  may  accumulate  behind 
the  obstruction.  When  this  occurs,  the  pelvis  of  the  kidney 
is  converted  into  a  sac  resembling  an  abscess.  If  these  ob- 
structions are  permanent,  frequently  an  opening  is  made 
through  the  walls  of  the  dilated  portion  and  the  contents 
of  the  sac  are  discharged  into  the  adjacent  tissue ;  or,  in- 
flammation may  be  established  around  the  distended  pelvis, 


522  MORBID  ANATOMY. 

adhesions  may  form,  and  the  contents  may  be  discharged 
externally  by  a  process  of  ulceration.  In  the  same  manner 
an  opening  may  be  made  into  an  intestine,  or  into  some  of 
the  other  hollow  viscera.  Under  these  circumstances  the 
affected  kidney  will  become  very  much  enlarged. 

When  the  obstructions  are  temporary,  as  they  give  way, 
the  contents  of  the  sac  are  discharged  into  the  bladder 
through  the  ureter,  after  which  repeated  obstructions  or 
accumulations  may  occur.  Sometimes  these  retained  accu- 
mulations undergo  entire  absorption,  and  we  have  remain- 
ing a  thick  cicatricial  tissue,  with  the  normal  kidney  tissue 
entirely  obliterated,  and  the  ureter  transformed  into  a  ten- 
dinous cord.  Under  such  circumstances  the  healthy  kidney 
becomes  increased  in  size  and  performs  in  a  very  satisfactory 
manner  the  function  of  both  kidneys,  and  the  patient  may 
live  for  many  years.  Again,  in  certain  cases,  the  accumula- 
tion in  the  kidney  is  changed  into  a  cheesy  material  and 
presents  an  appearance  similar  to  that  which  was  formerly 
called  tubercular  deposit.  Mingled  with  this  cheesy  mass 
may  be  found  the  salts  of  the  urine,  which  cause  it  to  have 
a  sandy  feel. 

ETIOLOGY. — The  causes  of  pyelitis  are  numerous.  It  is 
seldom  if  ever  a  primary  disease.  Sometimes,  though  very 
rarely,  exposure  to  cold  will  cause  slight  catarrhal  pyelitis. 

First. — The  most  frequent  cause  is  the  presence  of  calculi, 
or  any  foreign  substance,  in  the  pelvis  of  the  kidney. 
Under  such  circumstances  the  pyelitis  is  secondary  to  me- 
chanical irritation. 

Second. — Pyelitis  may  occur  as  the  result  of  the  irritation 
produced  by  the  decomposition  of  urine  retained  in  the 
pelvis  of  the  kidney,  as  a  consequence  of  some  obstruction 
to  its  normal  outlet.  For  instance,  an  enlarged  prostate 
gland,  or  an  urethra!  stricture,  causes  more  or  less  obstruc- 
tion to  the  passage  of  urine  from  the  bladder,  and  as  a 
result  of  the  retention  of  urine  in  the  bladder  cystitis  is  de- 
veloped, and  the  inflammation  of  the  mucous  surface  of  the 
bladder  may  extend  to  the  ureters,  and  from  the  thickening 
of  their  mucous  lining  and  the  diminution  of  their  calibre, 
the  passage  of  urine  from,  the  kidneys  to  the  bladder  is  ob- 


PTELITIS.  523 

structed,  and  there  is  not  only  retention  of  urine  in  the 
bladder,  but  also  in  the  pelvis  of  the  kidneys.  As  a  result 
of  such  retention,  the  urine  undergoes  decomposition,  the 
urea  is  changed  into  carbonate  of  ammonia  and  water, 
the  carbonate  of  ammonia  acts  as  an  irritant  and  excites 
inflammation  of  the  lining  membrane  of  the  pelvis,  and 
thus  pyelitis  is  developed. 

The  decomposition  of  urea  as  a  result  of  the  absorption 
of  the  ammonia,  may  be  sufficient  to  give  rise  to  a  condition 
which  has  received  the  name  of  ammonicemia. 

This  condition  is  not  uni'requently  mistaken  for  uraemia, 
yet  they  differ  widely  in  their  manifestations  and  the  dan- 
gers which  attend  their  development. 

In  ammonisemia  the  urine  when  voided  is  ammoniacal,  as 
is  also  the  breath  and  perspiration.  The  mucous  membrane 
of  the  mouth  is  dry  and  shining  ;  the  complexion  is  sallow, 
and  there  is  increasing  emaciation.  No  dropsical  accumula- 
tions are  present.  Convulsions  are  rare ;  chills  are  frequent. 
Vomiting  is  also  rare.  Death  is  usually  preceded  by  coma. 

In  uraemia,  the  characteristic  symptoms  are  convulsions, 
vomiting,  and  dropsy. 

The  development  of  the  train  of  symptoms  indicative  of 
ammonisemia,  accompanied  by  the  evidence  of  obstruction 
to  the  normal  outlet  of  the  urine,  should  cause  us  to  hesi- 
tate before  performing  any  operation,  especially  an  opera- 
tion for  relief  of  stricture  of  the  urethra. 

Third. — Pyelitis  occurs  not  unfrequently  in  connection 
with  that  class  of  diseases  which  depend  upon  blood-poison- 
ing. In  this  connection,  it  is  generally  a  complication  of 
the  acute  form  of  Blight's  disease,  and  is  not  severe  in 
character,  but  causes  bloody  urine  and  gives  evidence  of 
catarrhal  inflammation  of  the  pelvis. 

Fourth.—  Pyelitis  occasionally  occurs  in  consequence  of 
over-doses,  or  the  prolonged  use  of  certain  irritating  drugs, 
as  turpentine,  cantharides,  and  other  stimulating  diuretics. 

In  very  rare  instances,  pyelitis  seems  to  come  on  idio- 
pathically  from  exposure  to  cold  and  wet,  or  from  some  un- 
known cause.  Usually,  however,  it  is  secondary  to  antece- 
dent morbid  processes  or  mechanical  irritation. 


524  SYMPTOMS. 

SYMPTOMS. — In  the  majority  of  cases,  the  development  of 
pyelitis  is  preceded  or  accompanied  by  symptoms  due  to 
the  causes  which  produce  it,  such  as  renal  calculi,  diseases 
of  the  bladder,  etc. 

At  this  time,  I  shall  confine  myself  to  those  symptoms 
which  directly  attend  its  development.  Prominent  among 
these  is  pain  in  the  back.  This  is  present  in  the  mild  as 
well  as  in  the  severe  cases.  This  pain  may  have  its  point 
of  maximum  intensity  over  one  or  both  lumbar  regions.  It 
is  often  of  an  aching  character,  and  shoots  down  along  the 
course  of  the  ureters.  This  pain  is  usually  accompanied  by 
frequent  micturition,  and  when  it  is  very  intense,  the  void- 
ing of  urine  is  almost  incessant,  and  is  attended  by  severe 
pain. 

The  commencement  of  acute  pyelitis  is  usually  marked 
by  rigor,  and  in  that  chronic  form  in  which  temporary  ob- 
struction of  the  ureter  occurs,  frequent  rigors  are  present. 

Symptoms  of  hectic  fever  may  also  mark  the  occurrence 
of  permanent  obstruction  of  the  ureter  and  the  development 
of  that  condition  termed  pyonephrosis. 

There  is  usually  considerable  lassitude  attending  the 
progress  of  pyelitis,  and  when  the  disease  is  due  to  the 
presence  of  a  calculus,  the  patient  ordinarily  suffers  more 
or  less  pain  upon  exertion  or  change  of  position. 

All  of  these  symptoms  are  accompanied  by  changes  in 
the  urine,  and  these  changes  are  the  real  signs  of  the 
disease,  and  must  be  regarded  as  its  most  important  direct 
symptoms. 

URIISTE. — In  the  early  stage  of  the  disease,  the  urine  con- 
tains blood  mixed  with  mucus  and  epithelial  cells  from  the 
pelvis  and  infundibula. 

The  presence  of  epithelial  cells  from  the  pelvis  of  the 
kidney,  which  are  readily  distinguished  from  epithelium  of 
iny  other  portion  of  the  urinary  track  by  their  characteristic 
shape  and  appearance,  is  the  most  certain  diagnostic  indica- 
tion in  the  early  stage  of  pyelitis.  The  urine  is  of  higher 
specific  gravity  than  normal,  ranging  from  1025  to  1030,  and 
it  usually  retains  its  acid  reaction.  If,  therefore,  upon 
microscopical  examination  of  the  urine,  you  find  the  pecu- 


PYELTTIS.  52£ 

liar  epithelial  cells  of  the  pelvis  of  the  kidney,  with  some 
pus-cells  and  blood-globules  mingled  with  mucus,  and  the 
urine  is  acid,  you  may  be  certain  that  your  patient  is  suffer- 
ing from  acute  pyelitis. 

In  the  more  advanced  stages,  the  characteristic  epithelium 
is  to  a  great  extent  replaced  by  an  abundance  of  pus-cells, 
but  the  urine  retains  its  acid  character.  If  sacculation  of 
the  kidneys  is  developed,  the  mingled  pus  and  urine  in  the 
sacculated  portion  is  liable  to  undergo  decomposition,  and 
the  urine  will  become  ammoniacal. 

Albumen  is  present  in  proportion  to  the  amount  of  pus 
and  blood. 

In  the  advanced  stage  of  pyelitis,  if  the  urinary  channels 
remain  free,  the  discharge  of  pus  is  constant  and  free.  If, 
however,  the  ureter  (if  the  disease  is  confined  to  one  kid- 
ney) becomes  blocked  up  by  a  calculus  or  any  other  sub- 
stance, for  a  time  the  urine  may  become  quite  natural,  but 
on  the  removal  of  the  obstruction,  a  copious  flow  of  puru- 
lent urine  follows.  This  may  be  repeated  from  time  to 
time,  at  intervals  varying  from  a  few  days  to  a  few  months, 
or  the  obstruction  may  become  permanent.  If  the  obstruc- 
tion is  long- continued  or  becomes  permanent,  a  tumor 
develops  in  the  lumbar  region. 

If  the  pelvis  of  both  kidneys  is  affected,  and  there  is 
partial  or  complete  obstruction  of  one  side,  the  accumula- 
tion of  pus  in  the  urine  is  diminished,  but  not  entirely  pre- 
vented. 

The  development  of  a  pyonephrotic  tumor  in  the  lumbar 
region  is  a  later  event  in  chronic  pyelitis,  and  indicates 
complete  obstruction  of  the  ureter,  and  a  large  accumula- 
tion of  fluid  in  the  pelvis  of  the  kidney. 

The  existence  of  the  tumor  is  determined  by  the  presence 
of  bulging  between  the  crest  of  the  ilium  and  the  false  ribs 
on  the  right  or  left  side,  according  as  the  right  or  left  kid- 
ney is  involved.  As  a  consequence,  the  outline  of  the 
abdomen  is  rendered  unsymmetrical. 

On  palpation,  deep-seated  fluctuation  is  felt  over  the 
tumor,  which  usually  is  painful  and  tender  on  pressure. 

The  area  of  percussion  dulness  will  correspond  to  the 


526  DIFFERENTIAL   DIAGNOSIS. 

outline  of  the  tumor,  except  where  it  is  crossed  by  the 
colon.  With  these  physical  signs  present,  and  a  history  of 
pyelitis,  you  will  be  justified  in  resorting  to  the  exploring 
trocar  to  make  complete  your  diagnosis. 

DIFFERENTIAL  DIAGNOSIS. — The  diagnosis  of  pyelitis  in 
its  first  or  acute  stage,  rests  almost  exclusively  on  the 
presence  in  the  urine  (as  determined  by  the  microscope)  of 
the  characteristic  epithelium  of  the  pelvis  and  infundibula, 
mixed  with  blood-globules  and  mucus.  If  the  urine  con- 
tains pus-cells  mixed  with  these  epithelial  cells,  it  indicates 
a  more  advanced  stage  of  the  disease.  The  presence  of  pus 
and  acid  urine,  with  pain  in  the  lumbar  region,  accompanied 
by  the  development  of  a  tumor  at  the  seat  of  pain,  which 
tumor  gradually  increases  in  size,  and  suddenly  disappears 
by  a  copious  discharge  of  pus  from  the  bladder,  which  dis- 
charge is  attended  by  a  sense  of  great  relief  to  the  patient, 
renders  the  diagnosis  of  pyonephrosis  very  certain.  If  the 
ureter  of  the  affected  kidney  is  permanently  obstructed, 
the  lumbar  tumor  is  liable  to  be  mistaken  for  hydronephro- 
sis,  an  hydatid  cyst,  or  a  perinephritic  abscess. 

The  exploring  trocar  will  very  quickly  remove  all  doubts, 
for  the  removal  of  a  small  quantity  of  the  fluid,  and  a  mi- 
croscopical examination  of  it  after  its  removal,  will  de- 
termine its  origin  and  character. 

When  pyelitis  occurs  as  a  complication  of  chronic  cystitis, 
an  enlarged  prostate  gland  or  urethral  stricture,  if  there  is 
no  tumor  in  the  lumbar  region,  it  is  often  impossible  to 
reach  a  positive  diagnosis  of  its  existence.  Under  these 
circumstances,  the  character  of  the  urinary  constituents  do 
not  very  much  assist  you.  If,  however,  the  quantity  of 
pus  is  large,  the  urine  slightly  acid,  the  loins  painful  on 
pressure,  and  the  febrile  movements  constant,  with  rapid 
loss  of  flesh  and  strength,  you  have  good  reason  to  believe 
that  chronic  pyelitis  has  been  added  to  diseases  of  the 
bladder  and  urethra. 

PROGNOSIS. — The  prognosis  in  pyelitis  depends  to  a  very 
great  extent  upon  the  nature  of  the  exciting  cause. 

In  simple  catarrhal  pyelitis,  not  connected  with  extensive 
disease  of  other  portions  of  the  urinary  apparatus,  the 


PYELITIS.  527 

prognosis  is  not  unfavorable.      If,   however,   the  disease 
affects  both  kidneys,  and  has  reached  the  purulent  stage, 
whatever  may  have  been  its  cause,  the  prognosis  is  bad. 
^  When  the  disease  is  confined  to  one  side,  recovery  is  pos- 
sible, although  one  kidney  may  be  completely  destroyed. 

Pyelitis  may  be  regarded  as  a  hopeless  disease  when  it  is 
secondary  to  an  enlarged  prostate  gland,  extensive  chronic 
cystitis,  urethral  stricture,  and  cancer  of  the  kidney.  It  is 
exceedingly  grave  when  it  depends  upon  renal  calculi  and 
hydatids,  although  it  is  not  necessarily  fatal. 

The  issues  of  a  pyonephrosis  are  uncertain ;  the  various 
directions  in  which  a  sac  may  burst  determine  to  a  great 
extent  its  termination.  Rupture  into  the  peritoneal  or 
thoracic  cavities  is  speedily  fatal.  Recovery  is  possible 
if  the  rupture  takes  place  externally,  or  into  an  intestine. 
Sometimes,  when  the  sac  does  not  rupture,  patients  die 
from  the  exhaustion  caused  by  the  long-continued  dis- 
charge. Recovery  may  be  reached  by  a  gradual  diminution 
of  the  discharge,  and  a  final  contraction  and  obliteration  of 
the  sac,  provided  the  other  kidney  is  unaffected. 

TKEATMEOT.—  The  first  thing  in  the  treatment  of  pyelitis 
is,  if  possible,  to  remove  its  cause. 

If  the  attack  is  an  acute  one,  and  at  the  onset  of  the 
disease  the  fever  is  considerable,  the  pain  in  the  lumbar 
region  severe,  and  the  urine  bloody,  wet  cups  should  be 
freely  applied  to  the  loins,  followed  by  a  hot  bath  and  a 
sufficiently  large  hypodermic  of  morphine  to  entirely  relieve 
the  patient  of  pain.  The  patient  should  drink  freely  of 
alkaline  fluids  and  should  be  kept  in  bed.  In  chronic  pye- 
litis, when  the  secretion  of  pus  is  abundant,  astringents  may 
be  employed  to  diminish  the  purulent  secretion.  Attention 
should  be  paid  to  the  general  health  of  the  patient.  Cod- 
liver  oil  and  quinine  should  be  administered  with  a  nutri- 
tious and  non-stimulating  diet.  A  residence  at,  and  prolonged 
use  of  the  waters  of  some  alkaline  spring,  will  often  be  found 
of  great  service. 

When  a  tumor  exists  and  can  readily  be  reached  through 
the  integument,  aspiration  may  be  performed,  after  which 
the  question  of  a  free  permanent  external  opening  will 


fi2S  MORBID   ANATOMY. 

present  itself,  and  must  be  decided  by  the  peculiarities  of 
each  case. 

HYDRONEPHROSIS. 

There  is  another  affection  of  the  pelvis  of  the  kidneys 
which  is  non-inflammatory  in  its  nature,  concerning  which 
I  will  say  a  few  words.  Whenever  the  flow  of  urine  through 
the  ureters  into  the  bladder  is  permanently  obstructed,  the 
urine  collects  in  the  pelvis  and  infundibula  of  the  kidney, 
compressing  the  renal  substance,  which  becomes  partially 
or  completely  atrophied,  so  that  after  a  time  the  kidney  is 
converted  into  a  sac  or  pouch.  This  condition  has  received 
the  name  of  hydronephrosis.  The  dilatation  may  affect  the 
ureter  and  pelvis,  or  only  the  pelvis. 

MORBID  ANATOMY. — In  a  kidney  that  is  the  seat  of 
moderate  hydronephrosis,  the  papillae  become  flattened, 
hardened,  and  shrunken,  and  gradually  disappear.  The 
remaining  portion  of  the  renal  substance  gradually  dimin- 
ishes from  the  pressure  and  becomes  more  or  less  tough  and 
resistant.  In  extreme  cases,  the  kidney  substance  finally 
entirely  disappears,  and  the  kidney  is  converted  into  a  large 
multilocular  cyst.  At  times  such  a  cyst  attains  a  size  as 
large  as  a  child's  head.  Sometimes  healthy  kidney  substance 
will  be  found  in  its  walls.  That  portion  of  the  ureter  which  is 
the  seat  of  dentation  may  reach  the  size  of  a  small  intestine, 
its  walls  become  greatly  thickened,  and  it  may  become  con- 
voluted. The  fluid  contents  of  hydronephrotic  cysts  are 
generally  altered  urine.  It  is  much  more  watery  than 
normal  urine,  containing  more  or  less  of  the  urinary  salts  ; 
it  may  also  contain  blood,  pus,  epithelium,  and  some 
albumen. 

ETIOLOGY. — Closure  of  an  ureter  which  gives  rise  to  a 
hydronephrosis  may  be  due  to  compression  of  the  ureter  by 
a  tumor  external  to  its  walls,  or  to  the  impaction  of  a  cal- 
culus in  its  calibre,  or  to  inflammation  which  has  caused 
adhesion  of  its  walls  and  complete  obliteration  of  its  cali- 
bre. A  moderate  degree  of  dilatation  of  the  ureter  some- 
times is  the  result  of  an  impediment  to  the  discharge  of 
urine  from  the  bladder ;  when  this  is  the  case,  the  pelvic 


HYDRONEPIIEOSIS.  529 

dilatation  is  bilateral,  and  can  never  become  very  extensive 
without  destroying  life,  for  if  the  pressure  is  very  great,  it 
will  completely  close  the  papillae  of  the  kidneys  and  en- 
tirely suppress  the  urinary  secretion. 

SYMPTOMS.— The  symptoms  of  hydronephrosis  mainly 
depend  upon  the  nature  of  its  anatomical  cause  and  on  the 
extent  of  the  dilatation. 

If  the  sac  is  small  and  the  opposite  kidney  healthy,  there- 
may  be  no  symptoms  to  indicate  its  existence ;  there  will 
be  no  diminution  in  the  urinary  secretion,  as  the  healthy 
kidney  performs  the  work  of  the  diseased  organ,  and  there 
may  be  no  pain  in  the  lumbar  region.  As  soon,  however, 
as  the  tumor  in  the  abdomen  attains  sufficient  size  to  be 
readily  felt,  the  existence  of  hydronephrosis  may  be  de- 
termined by  it.  This  tumor  causes  no  pain  nor  any  incon- 
venience, except  by  its  bulk. 

If  the  obstruction  to  the  escape  of  urine  from  the  kidney 
is  temporarily  removed,  its  removal  will  be  followed  by  a 
sudden  diminution  and  disappearance  of  the  tumor,  co- 
incident with  a  sudden  discharge  of  a  large  quantity  of 
urine.  Such  an  occurrence  is  almost  pathognomonic  of 
hydronephrosis,  and  it  is  upon  this  you  must  mainly  rely 
in  making  your  diagnosis. 

DIFFERENTIAL  DIAGNOSIS. — Hydronephrotic  tumors  may 
be  confounded  with  ovarian  cysts,  ascites,  hydatid  cysts, 
pyonephrosis.  They  are  distinguished  from  ovarian  cysts 
by  the  presence  of  the  colon  in  front  of  the  swelling,  and  by 
the  absence  of  tympanitic  percussion  in  the  lumbar  region. 

Single  hydronephrosis  is  distinguished  from  ascites  by  the 
non-existence  of  dulness  in  both  lumbar  regions,  and  in 
ascites,  when  the  position  of  the  patient  is  changed,  there 
is  a  change  in  the  level  of  dulness. 

It  is  quite  impossible  to  distinguish  hydronephrosis  from 
a  hydatid  cyst,  unless  the  hydatid  vesicles  are  found  in  the 
urine,  or  the  hydatid  fremitus  is  present. 

It  is  distinguished  from  pyonephrosis  by  the  non-purulent 
character  of  the  urine,  and  by  the  existence  of  less  severe 
constitutional  symptoms,  and  by  evidencing  no  signs  of 
suppuration. 
34 


530  CYSTIC   KIDNEYS. 

PROGNOSIS. — The  prognosis  is  more  favorable  in  this  than 
in  any  other  form  of  renal  tumor. 

When  only  one  kidney  is  involved  (which  is  usually  the 
case),  life  may  be  indefinitely  prolonged,  and  there  is 
always  a  possibility  that  spontaneous  evacuation  of  the  sac 
may  occur. 

If  the  healthy  kidney  becomes  the  seat  of  any  form  of 
nephritic  degeneration,  the  prognosis  suddenly  becomes  un- 
favorable ;  or,  if  the  impediment  which  has  obstructed  one 
ureter  extends  so  as  to  prevent  the  flow  of  urine  from  both 
kidneys  into  the  bladder,  ursemic  symptoms  will  be  devel- 
oped, and  the  death  of  the  patient  will  soon  follow  their 
development. 

TREATMENT. — In  hydronephrosis,  the  principal  thing  to 
be  accomplished  by  treatment  is  the  evacuation  of  the 
tumor.  To  accomplish  this  result,  it  should  be  carefully 
manipulated.  This  can  readily  be  done,  as  the  tumor 
generally  causes  no  pain.  If  this  does  not  cause  the  evacu- 
ation of  the  tumor,  resort  to  aspiration.  I  now  have  a  case 
under  observation  in  which  aspiration  has  twice  been  per- 
formed with  complete  relief  to  the  patient,  and  the  aspira- 
tion has  not  been  followed  by  any  unpleasant  symptoms. 
You  have  nothing  to  hope  from  medicinal  treatment. 

CYSTIC  KIDNEYS. 

Cystic  degeneration  of  the  kidneys  is  not  unfrequently 
met  with  at  autopsies,  but  it  is  of  very  little  clinical  im 
portance,  for  if  the  cysts  are  of  small  size  it  rarely  mani 
fests  itself  during  life  by  any  symptoms. 

This  form  of  degeneration  may  be  of  congenital  origin, 
and  both  kidneys  may  be  found  converted  into  a  mass  of 
cysts  of  sufficient  size  to  entirely  fill  the  abdominal  cavity  ; 
such  conditions  are  usually  associated  with  other  malforma- 
tions. 

Again,  cysts  may  be  found  scattered  through  kidneys  that 
are  otherwise  healthy.  You  may  find  a  number  of  cysts, 
varying  in  size  from  a  small  pea  to  a  hickory  nut,  usually 
situated  in  the  cortical  substance  near  to  the  surface. 


"RENAL   CONCRETIONS.  531 

These  cysts  may  contain  clear  albuminous  fluid,  sometimes 
gelatinous  in  character,  containing  phosphates,  carbonates, 
cholesterin,  and  very  rarely  urea  and  uric  acid. 

We  have  no  positive  knowledge  as  to  the  manner  in  which 
these  formations  are  produced,  although  it  is  supposed  that 
they  are  the  results  of  dilatation  of  the  kidney  tubules. 

Again,  in  the  different  forms  of  Bright' s  disease,  cysts  are 
frequently  found  in  kidneys  that  are  in  the  stage  of  atrophy. 
To  these  reference  has  previously  been  made. 

There  is  a  very  rare  form  of  general  cystic  degeneration 
of  both  kidneys,  found  in  adults,  which  is  only  of  interest 
on  account  of  its  rarity.  In  this  form  the  kidneys  are 
greatly  enlarged,  sometimes  weighing  several  pounds,  and 
are  classed  among  abdominal  tumors. 

This  cystic  degeneration  is  of  such  rare  occurrence,  that  I 
will  not  detain  you  with  its  farther  description. 

RENAL   CONCRETIONS. 

The  causes  of  the  different  forms  of  renal  disease  which 
have  been  engaging  our  attention  to-day,  are  intimately  con- 
nected with  the  formation  of  renal  concretions.  These  con- 
cretions greatly  vary  in  shape,  and  widely  differ  in  their 
composition.  They  may  be  deposited  in  the  tubes  of  the 
pyramids,  in  the  cortical  substance,  or  in  the  pelvis  of  the 
kidney.  Their  development  occurs  at  any  age  ;  they  are  met 
with  in  the  kidney  of  the  new-born  infant,  and  in  the 
kidney  of  the  very  aged. 

MORBID  ANATOMY.— In  the  kidneys  of  infants  dying 
within  forty-eight  hours  after  birth,  brownish  strise  of 
amorphous  urates  will  invariably  be  found  running  from 
the  papillae  to  the  base  of  the  pyramids. 

In  the  kidneys  of  the  adult,  urate  of  soda  may  be  found 
deposited  in  white  lines  and  spots  in  the  pyramids  and 
cortical  substance.  This  deposit  may  take  place  in  the  form 
of  crystals,  both  in  the  tubes  and  in  the  intertubular  struc- 
ture, and  is  always  associated  with  a  gouty  diathesis. 

Carbonate  and  phosphate  of  lime  may  be  found  deposited 
in  the  tubes  and  pyramids  of  the  kidneys  of  old  people,  or 
in  connection  with  diseases  of  the  bones. 


532  MORBID   ANATOMY. 

These  different  forms  of  urinary  concretions  may  be  per- 
manently impacted  in  the  uriniferous  tubes  and  render  them 
impervious,  and  thus  cysts  may  be  developed,  or  they  may 
be  washed  down  the  tubes  by  the  urine,  and  finally  be 
deposited  in  the  inf undibula  and  pelvis  of  the  kidney. 

They  vary  very  greatly  in  number  and  size.  A  kidney 
may  contain  one  concretion  or  a  large  number  of  these  con- 
cretions. They  usually  vary  in  size,  from  a  pin' s  head  to  a 
hazel-nut ;  the  larger  ones  may  fill  the  whole  pelvis  of  the 
kidney.  If  a  concretion  becomes  impacted  in  the  pelvis  of 
the  kidney,  it  may  become  of  very  large  size,  weighing  one 
or  two  ounces.  The  smaller  calculi  pass  through  the  ureters 
into  the  bladder  and  are  discharged  ;  the  larger  ones  may 
permanently  obstruct  the  ureters  and  become  the  cause  of 
pyonephrosis  and  hydronephrosis.  Consequently,  the  ana- 
tomical changes  produced  by  renal  concretions  vary ;  they 
may  cause  pyelitis,  pyonephrosis,  hydronephrosis,  abscess, 
or  they  may  excite  parenchymatous  nephritis. 

ETIOLOGY. — The  causes  of  the  different  concretions  found 
in  the  kidneys  are  very  obscure.  Uric  acid  is  most  fre- 
quently met  with  in  infants.  The  deposits  of  lime  and 
triple  phosphates  are  most  frequently  met  with  in  adults. 

Certain  conditions  are  supposed  to  be  favorable  to  the 
development  of  renal  calculi,  but  the  exact  nature  of  the 
urinary  changes  has  not  as  yet  been  determined.  In  most 
cases,  calculi  developed  in  the  pelvis  of  the  kidney  have  some 
foreign  substance  as  their  nuclei.  These  nuclei  may  be  pus, 
blood,  epithelium,  or  grains  of  pigment.  The  composition  of 
the  remaining  portion  of  the  calculi  depends  upon  the  vary- 
ing conditions  which  attend  their  development. 

SYMPTOMS. — The  symptoms  which  mark  the  development 
of  renal  calculi  vary.  In  some  instances  they  are  well 
marked ;  in  other  instances  they  are  very  obscure,  so 
obscure  that  you  cannot  detect  the  presence  of  calculi. 
Usually,  the  existence  of  renal  calculi  is  indicated  by  an 
aching  pain  in  the  loins,  which  frequently  shoots  into  the 
testicles  and  down  the  thighs,  by  an  itching  at  the  end  of 
the  penis,  and  by  a  frequent  desire  to  urinate.  The  urine 
often  contains  pus,  blood,  and  epithelium  from  the  pelvis 


EE1STAL   CONGESTIONS.  533 

of  the  kidney.  These  symptoms  are  usually  aggravated 
by  anything  which  disturbs  the  position  of  the  calculi, 
especially  by  violent  exercise,  or  by  jolting  in  riding,  horse- 
back riding,  etc. 

The  symptoms  often  assume  the  characteristics  of  "renal 
colic,"  due  to  the  passage  of  a  calculus  along  the  ureter  to 
the  bladder ;  this  occurs  after  violent  exercise,  or  without 
any  assignable  cause. 

The  passage  of  a  calculus  along  the  ureter  into  the  blad- 
der is  marked  by  sudden  and  intense  pain  in  the  region  of 
the  affected  kidney.  This  pain  radiates  in  various  direc- 
tions, but  mainly  towards  the  hypogastrium,  testis,  inside 
of  the  thigh,  and  end  of  the  penis.  There  is  a  constant 
desire  to  micturate,  but  the  urine  is  scanty  or  suppressed, 
and  what  is  passed  is  of  a  high  color,  often  bloody,  and  is 
discharged  in  drops,  the  individual  at  the  time  experiencing 
a  painful,  burning  sensation.  The  testicle  on  the  affected 
side  is  retracted.  As  the  pain  increases  in  severity,  the 
patient  rolls  from  side  to  side,  and  shrieks  with  pain.  His 
countenance  becomes  pale,  and  the  surface  of  the  body  is 
covered  with  a  cold  perspiration.  The  pulse  is  small,  and 
the  hands  and  feet  are  cool.  The  severe  paroxysms  of  pain 
are  attended  by  violent  and  frequent  vomitings.  Great 
anxiety  attends  these  symptoms,  and  if  the  patient  is  of  a 
very  nervous  temperament,  convulsions  may  occur.  If  the 
attack  is  prolonged,  there  is  more  or  less  fever  present ; 
sometimes  it  attains  a  high  degree. 

The  duration  of  these  attacks  varies.  Sometimes  they  are 
only  of  a  few  hours'  duration  ;  at  other  times  they  may  be 
prolonged  for  days;  again,  temporary  remissions  may 
occur,  and  these  may  be  followed  by  renewed  and  violent 
exacerbations. 

If  the  calculus  reaches  the  bladder,  the  symptoms  usually 
subside  suddenly,  with  a  sense  of  intense  relief,  and  the 
patient  is  often  conscious  that  something  heavy  has  passed 
into  the  bladder.  Occasionally,  the  concretion  becomes 
impacted  in  some  portion  of  the  ureter.  In  such  cases, 
the  subsidence  of  the  symptoms  is  more  gradual  and  less 
complete,  and  signs  of  hydronephrosis  foUow. 


534  DIFFERENTIAL   DIAGNOSIS. 

Renal  calculi  may  attain  to  a  large  size  and  destroy 
extensive  portions  of  the  kidney,  and  yet  not  a  single 
symptom  may  be  present  to  indicate  their  existence. 

Again,  symptoms  of  renal  concretion  may  exist  for  a 
long  time,  until  finally  atrophy  of  the  kidney  occurs  ;  or 
they  may  become  encysted  and  cease  to  irritate  the  kidney 
or  impede  the  flow  of  urine. 

DIFFERENTIAL  DIAGNOSIS. — Renal  concretions  may  be 
confounded  with  neuralgia  of  the  lower  intercostal  and 
abdominal  nerves.  In  both,  the  seat  of  pain  is  the  same, 
and  the  neuralgic  pains  are  often  severe  and  paroxysmal ; 
but  renal  concretion  may  be  distinguished  by  the  presence 
of  pus,  blood,  and  epithelium  in  the  urine. 

The  passage  of  blood-clots  or  hydatids  through  the 
ureter,  causing  renal  colic,  cannot  be  distinguished  from 
the  passage  of  renal  calculi,  except  the  antecedent  history 
is  known  and  appreciated. 

When  renal  concretions  are  latent,  or  are  attended  by 
obscure  lumbar  pains,  and  slight  disturbance  on  mictu- 
rition, repeated  and  careful  examinations  of  the  urine  are 
the  only  means  by  which  we  may  arrive  at  a  correct  diag- 
nosis. Frequently  the  abnormal  conditions  of  the  urine 
which  indicate  the  presence  of  renal  concretions,  are  present 
only  after  violent  exercise. 

PROGNOSIS. — In  renal  concretions  the  prognosis  is  good, 
unless  the  calculi  become  impacted  and  obstruct  the  ureter, 
or  are  of  too  large  size  to  pass  through  the  ureter  to  the 
bladder.  In  these  conditions,  the  prognosis  is  the  same  as 
in  similar  conditions  in  pyelitis,  pyonephrosis,  and  hydro- 
nephrosis. 

TREATMENT. — The  treatment  of  renal  concretion  in  the 
interval  between  the  paroxysms  which  take  place  during 
the  passage  of  renal  calculi,  will  depend  upon  the  changes 
which  we  infer  have  taken  place  in  the  kidnej^s. 

I  shall  not  detain  you  with  the  enumeration  of  the  differ- 
ent theories  which  have  been  advanced  in  regard  to  the 
dissolving  of  these  concretions,  for  none  of  them  are  of 
practical  importance.  The  means  to  be  employed  for  the 
relief  of  the  kidney-changes  due  to  the  pressure  and  irri- 


KEKAL   COETCKETIONS.  535 

tation  of  these  concretions,  have  been  considered  under 
pyelitis  and  pyonephrosis. 

The  paroxysms  which  attend  the  passage  of  renal  concre- 
tions from  the  kidney  to  the  bladder,  may  be  relieved  by 
the  free  administration  of  opium,  warm  baths,  and  the 
application  of  hot  poultices  to  the  loins  and  abdomen.  In 
some  instances,  when  the  pain  is  intense  and  the  vomiting 
constant,  inhalation  of  chloroform  will  be  found  to  give  the 
most  speedy  and  sometimes  permanent  relief. 

Change  in  the  position  of  the  patient  and  manipulation 
of  the  abdomen  along  the  course  of  the  ureters  may  some- 
times dislodge  a  calculus,  and  facilitate  its  passage  into  the 
bladder. 

NEW  GROWTHS  IN  THE  KIDNEY. 

There  are  many  varieties  of  new  growths  in  the  kidney. 
Cancer  is  the  only  one  which  has  any  special  clinical  sig- 
nificance. I  shall  only  speak  of  the  others  as  possible 
occurrences. 

Luksemic  tumors  are  occasionally  met  with  as  small 
whitish  masses,  developed  in  the  inter- tubular  tissue. 
They  are  composed  of  lymphoid  cells,  and  are  always  asso- 
ciated with  similar  growths  in  the  other  viscera. 

Syphilitic  gummata  are  also  met  with  in  the  kidneys  in 
the  form  of  small  nodules,  in  connection  with  similar  devel- 
opments in  the  other  organs. 

Fibroma  may  appear  in  the  pyramids  of  kidneys  in  the 
form  of  small,  white,  fibrous  nodules.  The  remaining  por- 
tion of  the  kidney  will  be  normal,  or  the  seat  of  parenchy- 
matous  nephritis. 

Lipoma  includes  those  accumulations  of  fatty  tissue  which 
are  sometimes  developed  around  the  capsule  of  the  kidney, 
and  in  the  pelvis  of  atrophied  kidneys  ;  sometimes,  in  the 
cortical  substance  beneath  the  capsule,  small,  rounded, 
fatty  tumors  are  found. 

Tubercles  are  only  met  with  in  the  kidneys  in  connection 
with  general  tuberculosis.  They  take  the  form  of  small, 
miliary,  gray,  or  cheesy  granulations.  They  have  no  clini- 
ical  significance. 


536  MORBID  ANATOMY. 

RENAL  CANCER. 

Renal  cancer  may  occur  as  a  primary  or  secondary  affec- 
tion. When  secondary,  its  developments  usually  are  of 
small  size,  and  may  occur  in  both  kidneys. 

MORBID  ANATOMY. — Generally  both  forms  of  cancer  of 
the  kidney  are  of  the  medullary  variety,  and  develop  in  the 
form  of  circumscribed  nodules  in  the  cortical  substance. 
Sometimes  a  whole  kidney  is  transformed  into  a  cancerous 
mass,  which  attains  an  enormous  size,  filling  up  a  large 
portion  of  the  abdominal  cavity. 

Cancer  of  the  kidney  is  very  often  associated  with  can- 
cer of  the  testicle.  The  minute  anatomical  changes  that 
take  place  in  cancerous  developments  in  the  kidney,  are 
similar  to  those  which  occur  in  cancerous  developments  in 
the  other  organs  of  the  body,  which  I  have  fully  considered 
in  another  connection.  I  shall  not  detain  you  with  their 
recapitulation. 

ETIOLOGY. — The  etiology  of  cancer  of  the  kidney  is  as 
obscure  as  the  general  etiology  of  cancer.  In  a  large  pro- 
portion of  cases,  it  undoubtedly  depends  either  upon  hered- 
itary taint  or  local  infection. 

SYMPTOMS. — Cancer  of  the  kidney  often  for  a  long  time 
remains  latent.  Its  development  is  marked  by  gradual 
emaciation,  for  which  no  cause  can  be  assigned.  It  may 
not  be  attended  by  pain  in  the  lumbar  region ;  if  pain  is 
present,  it  is  not  characteristic.  There  may  be  no  change 
in  the  renal  secretion. 

As  the  disease  advances,  and  the  cancerous  mass  reaches 
a  large  size,  it  can  be  felt  through  the  abdominal  walls. 
The  form  of  the  tumor  and  its  immobility  will  enable  you 
to  distinguish  it  from  enlargements  of  the  liver  or  spleen. 
Very  large  cancers  of  the  right  kidney  may  displace  the 
liver  upward. 

Hsematuria  and  albuminous  urine  are  sometimes  present. 
When  hsematuria  is  present,  it  is  constant,  and  continues 
for  a  long  time. 

In  the  advanced  stage,  the  complexion  assumes  the  char- 
acteristic cancerous  appearance. 


RENAL   CANCER.  537 

PROGNOSIS.— The  prognosis  in  cancer  of  the  kidney  is 
bad.  Death  is  reached  either  by  the  exhaustion  produced 
by  repeated  and  profuse  hemorrhages,  or  as  a  consequence 
of  some  intercurrent  disease,  as  acute  parenchymatous 
nephritis  of  the  unaffected  kidney,  or  from  the  invasion  of 
other  vital  organs  by  secondary  cancer. 

TREATMENT. — The  treatment  is  palliative.  The  principal 
objects  to  be  gained  are  the  relief  of  distressing  symptoms, 
and  the  sustaining  of  the  vital  powers. 

Parasites  in  tlie  ~kldney  are  occasionally  met  with,  the 
most  frequent  of  which  is  the  echinococcus. 

The  cysts  of  the  echinococcus  are  similar  to  those  found 
in  the  liver  and  other  organs.  Sometimes  they  are  of 
immense  size.  Generally  they  are  imbedded  in  the  fibrous 
capsule  of  the  kidneys.  They  may  atrophy,  or  occasion 
inflammation  and  suppuration,  and  rupture  into  the  peri- 
toneal cavity,  intestines,  or  pelvis  of  the  kidney. 

Their  development  may  be  unattended  by  any  appreciable 
symptoms. 

A  diagnosis  can  be  made  when  an  irregular  nodulated 
tumor  can  be  felt  in  the  region  of  the  kidney,  which  is 
accompanied  by  cysts  or  the  traces  of  echinococcus  in  the 
urine. 

The  cysticercus  cellulosus  and  the  strongylus  gigas  are 
parasites  of  rare  occurrence.  They  are  sometimes  found 
imbedded  in  the  kidney. 

The  symptoms  which  attend  their  development,  and  the 
manner  in  which  they  gain  entrance  into  the  kidney,  are 
obscure. 


INDEX. 


PAGE 

Aneurism,  cardiac,  etiology  of 417 

' '        morbid  anatomy  of 417 

"        prognosis  of 417 

"        symptoms  of 417 

"  "        treatment  of 417 

Angina  pectoris,  definition  of 425 

"        differential  diagnosis  of 426 

"        etiology  of 426 

"        morbid  anatomy  of 425 

"        prognosis  of  427 

"  "        symptoms  of 436 

"  "        treatmentof 427 

Aortic  obstruction,  differential  diagnosis  of 330 

"  "  etiologyof 328 

"  "  morbid  anatomy  of 326-328 

"  physical  signs  of 329 

prognosis  of 331,  332 

symptoms  of 328 

"  "  treatment  of 332 

Aortic  regurgitation,  differential  diagnosis  of. 337,  338 

"  "  etiologyof 335 

morbid  anatomy  of 333-335 

"  "  physical  signs  of. 336,337 

"  "  prognosisof 338,339 

"  "  treatmentof 340,341 

Apoplexy,  pulmonary,  differential  diagnosis  of 105 

"  "  etiologyof 104 

"  u  morbid  anatomy  of 102 

u  "  physical  signs  of. 106 

u  prognosis  of 107 

"  symptoms  of. 105 

"  "  treatment  of. 1°7 

Asthma,  differential  diagnosis  of * 

"        etiology  of ^7 

"        morbid  anatomy  of * 

"        physical  signs  of * 

„  70 

prognosis  of 

"  symptoms  of. 67'  68 

"  treatment  of 70~73 

'«  "  depressants  in  the ' 

"  "  sedatives  in  the ' 

*•  "  Btimulants  in  the "& 


540  INDEX. 

PAGH 

Blight's  diseases,  divisions  of 454,  455 

"  "  prognosis  of 505,  506 

"  "  treatment  of 506 

"  "  "  bleeding  in  the 507 

"  "  "  climate  in  the 515,  518 

"  "  "  cod-liver  oil  in  the 515 

"  "  "  diaphoretics  in  the 508-510 

"  "  "  dietinthe 513 

"  "  "  digitalis  in  the 511 

11  "  "  dry  cups  in  the 512 

hydragogue  cathartics  in  the 512 

"  "  "  mercurials  in  the 507 

iodine  in  the 516 

"  "  "  iron  in  the 513 

Bronchi,  dilatation  of. 60,  61 

"  stenosis  of 61 

Bronchitis,  capillary,  acute,  definition  of 46 

"  physical  signs  of. 48 

"  "  "  prognosis  of 49 

"  "  "  symptoms  of. 46,  47 

u  "  "  treatment  of 49-51 

"  catarrhal,  acute,  differential  diagnosis  of 44 

"  "  "  etiology  of 42 

"  "  "  morbid  anatomy  of 41 

"  "  "  physical  signs  of 44 

"  "  "  prognosis  of 45 

"  "  "  symptoms  of 43 

"  "  "  treatment  of 45 

"  chronic,  definition  of 52 

"  "  "  differential  diagnosis  of 58 

"  "  "  etiology  of 54 

"  morbid  anatomy  of. 52,  53 

"  "  physical  signs  of 57 

"  "  prognosis  of 58 

"  "  "  symptoms  of 55,  56 

"  "  "  treatment  of 58,  60 

"  croupous  definition  of 62 

"  differential  diagnosis  of 64 

"  "  etiology  of 62 

"  morbid  anatomy  of 62 

croupous,  physical  signs  of 63 

"  prognosis  of 64 

"  "  symptoms  of 62 

"  "  treatment  of 65 

"  varieties  of 40 

Cardiac  degenerations 401 

"  diseases 287 

"  murmurs,  diagnosis  of 369-375 

"  neuroses 422 

Cancer,  cardiac 421 

"  pulmonary,  differential  diagnosis  of 119 

"  "  etiology  of 118 


INDEX.  541 

PAOB 

Cancer,  pulmonary,  morbid  anatomy  of  .........................................  118 

physical  signs  of  ............................................  119 

prognosis  of  ................................................  119 

symptoms  of  ...............................................  118 

"          treatment  of  ...............................................  119 

"        renal,  etiology  of  .......................................................  536 

"      morbid,  anatomy  of.  .............................................  536 

44  "      prognosis  of  .....................................................  536 

u         •  "      symptoms  of  ....................................................  536 

"  "      treatment  of  .....................................................  537 

Congestion,  pulmonary,  brown  induration  .......................................     99 

compensatory  ...........................................     99 

"  "  definition  of  ............................................     98 

differential  diagnosis  of  .............................  100,  101 

"  "  etiologyof  .............................  .................  100 

"  "  hypostatic  ..............................................     99 

morbid  anatomy  of  .....................................     98 

physical  signs  of  ........................................  110 

44  "  prognosis  of  ............................................  101 

44  splenization  .............................................     98 

symptoms  of  ...........................................  100 

44  «4  treatment  of  ........................................  100-102 

44  4t  varieties  of  .............................................     98 

Dilatation,  cardiac,  definition  of  ................................................  388 

"  "  differential  diagnosis  of  ......................................  396 

44  "  etiology  of  ..............................................  390-393 

44  "  morbid  anatomy  of  ..........................................  389 

44  •'  physical  signs  of  ........................................  394-396 

14  "  prognosis  of.  ................................................  396 

44  4l  stages  of  ....................................................  388 

»  4t  symptoms  of  ............................................  392-394 

«'  "  treatment  of  ...........................................  398-400 

Emphysema,  pulmonary,  definition  of  ...........................................     ' 

»  "  differential  diagnosis  of  .................................     88 

«4  "  etiologyof  ..........................................  83,  84 

»  4(  morbid  anatomy  of  ...................................  79-83 

'.  4l  physical  signs  of  .....................................  86-88 

«*  4t  prognosis  of  ...........................................     * 

«  «  senile  ..................  ...............................     83 

«  "  symptoms  of  ................   .......................  84-86 

"  "  treatment  of  .......................................  90~93 

7Q 

»  "  varieties  of  ............................................     ' 

194 
Empyema,  definition  of  ......................................  " 

14          differential  diagnosis  of  .............................................. 

etiologyof  .......  . 

44          morbid  anatomy  of 

•»   •        £ 
physical  signs  of 

44          prognosisof 


symptomsof  ............................  '"  ^  ' 

treatment  of  ........................  c  . 

Endocarditis,  acute,  definition  ............................................. 


542  ESTDEX. 

PAGE 

Endocarditis,  acute,  differential  diagnosis  of. 315 

"  "        etiology  of. 311,  312 

"  "        morbid  anatomy  of 310,  311 

"        physical  signs  of 314,  315 

"        prognosis  of 316 

"  "        symptoms  of 317 

11  "        treatment  of. 318 

chronic,  etiology  of 320 

"  "         morbid  anatomy  of 330-334 

"         prognosis  of 325 

"  "          symptoms  of 334 

"  "         treatment  of 325 

"  renal 535 

Gangrene,  pulmonary,  differential  diagnosis  of. 116,  117 

etiology  of 115 

morbid  anatomy  of 114 

physical  signs  of 116 

"  "  prognosis  of 117 

symptoms  of 115 

"  "  treatmentof 117 

Haemathorax,  definition  of 212 

symptoms  of 212 

Heart,  amyloid,  degeneration  of,  etiology  of 413 

morbid  anatomy  of 413 

"  "  "  symptomsof 414 

"  <l  "  treatmentof 414 

"  cysts  in  the 422 

"  fatty  degeneration  of,  definition  of 406 

u  "  differential  diagnosis  of 411 

"  "  "  "  etiology  of 407 

"  "  "  "  morbid  anatomy  of 406 

"  "  "  "  physical  signs  of 410 

"  "  "  "  prognosisoi 411 

"  "  "  "  symptomsof 408 

"  "  "  "  "  arcus  senilis  as  a 409 

"  "  "  "  "  pulseasa. 409 

"  "  "  "  treatmentof 412 

"  fibroma  of  the 421 

"  lipoma  of  the 421 

"  myoma  of  the 421 

"  muscular  atrophy  of,  definition  of. 414 

etiology  of 415 

"  "  "  morbid  anatomy  of 414 

prognosis  of. 415 

"  "  "  symptomsof 415 

"  "  "  treatmentof 415 

"  parasites  in  the 421 

u  rupture  of,  definition  of. 416 

"  "  etiology  of 416 

"  "  prognosis  of 416 

"  "  symptoms  of . . . ; 416 


INDEX.  543 

Heart,  rupture  of,  treatment  o£ 416 

tubercle  in  the 401 

Hemorrhage,  bronchial,  differential  diagnosis  of 113 

etiology  of. _  109 

morbid  anatomy  of €  108 

prognosis  of ^  no 

symptoms  of i§  109-112 

treatment  of _  H3 

renal,  etiology  of 439 

"      morbid  anatomy  of ..437    439 

"      prognosis  of. _  _  440 

symptoms  of. _  _  439 

"      treatment  of __  441 

Hydronephrosis,  definition  of ,  . .  533 

differential  diagnosis  of 539 

morbid  anatomy  of . .  533 

prognosis  of 530 

symptoms  of 539 

treatment  of 530 

Hydropericardium,  definition  of. 306 

etiology  of. 306 

prognosis  of 307 

treatment  of. 307 

Hydropneumothorax,  definition  of 204 

differential  diagnosis  of 208 

"  etiology  of 204-206 

morbid  anatomy  of. 204 

physical  signs  of 207,  208 

prognosis  of. 209 

symptoms   of 206 

"  treatment  of 209 

Hydrothorax,  definition  of 210 

diagnosis  of 211 

prognosis  of 211 

symptoms  of 210 

"  treatment  of 211 

Hypertrophy,  cardiac,  definition  of 376 

"  "        differential  diagnosis  of 384 

"  "        etiology  of. 378-381 

"  "        morbid  anatomy  of 377,  378 

"  "    •    physical  signs  of 332-384 

"  "        prognosis  of 385 

•'  u        symptoms  of 381,  384 

"  "        treatmentof 336 

"  "        varieties  of 376 

Infarctions,  pulmonary,  hemorrhagic 102,103 

Kidney,  amyloid,  differential  diagnosis  of 497 

"  "         etiology  of 490 

"  "         morbid  anatomy  of 402-404 

"  "         prognosis  of 495 

"  '«         stagesof 4t}2 


544  IXDEX. 

PAGE 

Kidney,  amyloid,  symptoms  of 491 

"  "  "  dropsy  as  a 493 

44  "  "  nervous 494 

44  "  "  urine  as  a 493 

"        cirrhotic,  differential  diagnosis  of 503 

44  "        etiology  of 496 

"  "        morbid  anatomy  of 465-469 

44  "        stages  of 465 

44  44        symptoms  of 497 

44  "  "  cardiac  hypertrophy  as  a 501 

44  4l  44  dropsy  as  a 500 

"  "  "  nervous 501 

44  "  4l  urine  as  a 499 

41        concretions  in  the,  differential  diagnosis  of 534 

41  "  44        etiology  of 532 

44        morbid  anatomy  of 531 

44  44        prognosis  of 534 

"  44  44       symptomsof 532 

»«  "  "  4<  painasa 533 

44  i4  "  4I  retracted  testicle  as  a 533 

44  '4  44        treatment  of 534 

44        congestion  of,  etiology  of 434 

"  "  morbid  anatomy  of 432-434 

44  prognosis  of 435 

"  symptoms  of 435 

44  "  treatment  of 436 

44        cystic 530 

44        diseases  of,  classification  of 432 

14        parasites  in  the 537 

14        parenchymatous  inflammation  of 455 

"  "  4l  amaurosis  in 486 

"  44  44  bronchitis  in 485 

"  44  4t  differential  diagnosis  of 487 

«  44  4I  etiology  of 469-473 

44  4t  44  endocarditis  in 485 

44  "  44  meningitis  in 485 

41  "  "  morbid  anatomy  of 455-461 

44  "  '4  pleurisy  in 485 

"  44  44  pneumonia  in 485 

«•  "  4l  prognosis  of 4.88-491 

"  "  44  symptoms  of '. 472 

"  4(  44  "  dropsy  as  a 482 

"  44  44  "  nervous 483 

«  «4  44  "  urine  as  a 479-482 

44        tubercle  in  the 535 

44        tumors  of,  fibroma 535 

"  u          lipoma 535 

44  44          lenkasmic 535 

"  "          syphilitic  gummata 535 

Laryngitis,  catarrhal,  acute,  definition  of 2 

44  4t  4<      differential  diagnosis  of 5 

44  "  4l      etiology  of 3 


INDEX.  545 


PAGE 


Laryngitis,  catarrhal,  acute,  morbid  anatomy  of 

"      symptoms  of 3    4 

"      treatment  of .., g 

"          chronic,  definition  of 7 

differential  diagnosis  of 9 

u        etiology  of 8 

"        morbid  anatomy  of 7 

"        symptoms  of § 

"        treatment  of 10  U 

"         croupous,  definition  of 15 

"        differential  diagnosis  of. 19 

"                 "        etiology  of 17 

u        morbid  anatomy  of 15  ig 

"        prognosis  of .  20 

"        symptoms  of 17-19 

"        treatment  of 21-23 

Larynx,  anaesthesia  of 35 

"        cartilages,  ossification  of 39 

"        hyperaesthesia  of 35 

"        new  formations  in,  definition  of , 35 

"          "              "               differential  diagnosis  of 38 

"          "              "               etiology  of 37 

"          "              "               morbid  anatomy  of. 36 

prognosis  of 89 

"          "              "               symptoms  of 38 

treatment  of 39 

"          "              "               varieties  of 39 

"        paralysis  of,  differential  diagnosis  of 31 

"             "          "    etiology  of 29 

"          "    morbid  anatomy  of 28 

"              "          "    prognosisof 31 

"          "    symptoms  of SO 

"              "          "    treatment  of 32 

"              "          "    varieties  of. 27 

"        spasm  of,  definition  of .  22 

"          differential  diagnosis  of. 34 

"                "          etiology  of 33 

"                "          morbid  anatomy  of 32 

"                "          prognosisof 34 

u                "          symptoms  of 33 

"                "          treatment  of 34 

"        nlcers  of,  etiology  of 25 

"  "          morbid  anatomy  of 23,  24 

"                "          prognosisof 26 

"               "          symptoms  of 25 

"                "          treatment  of. 36 

"                "          varietiesof 23 

Mitral  obstruction,  differential  diagnosis  of 3- 

»  "  "          ctiologyof 344 

«  »  »          morbid  anatomy  of. 342-344 

«  "  "          physical  signs  of 345 

»  "  "          prognosisof ^47 

35 


546  INDEX. 

PAGE 

Mitral  obstruction,  differential  diagnosis  of 344,  345 

"  "  treatment  of 347 

"       regnrgitant,  differential  diagnosis  of 355 

etiology  of 351 

"  morbid  anatomy  of 34S-350 

''  physical  signs  of 353-355 

prognosis  of 255,  356 

"  symptoms  of 251-353 

treatment  of 357-359 

Myocarditis,  definition  of 401 

"  etiology  of 403 

morbid  anatomy  of 40H03 

prognosis  of 405 

"  symptoms  of. 404 

treatment  of. 405 

(Edema  glottidis,    definition  of 11 

"        differential  diagnosis  of 13 

"  "        etiologyof. 12 

"        morbid  anatomy  of. 12 

"  "        symptoms  of. 12 

"        treatment  of. 13 

"       pulmonary,  definition  of 93 

"  "  differential  diagnosis  of 95,  96 

"  "  etiologyof 94 

morbid  anatomy  of 93 

physical  signs  of 95 

prognosis  of 96 ' 

"  "  symptoms  of 94 

"  "  treatment  of 96,  97 

Palpitation,  cardiac,  nervous,  differential  diagnosis  of 424 

"  "  "          etiologyof 422 

"  "  "          morbid  anatomy  of 422 

"  "  "          prognosisof 424 

"          symptoms  of 423 

"  "  "          treatment  of 424 

Pericarditis,  acute,  definition  of 288 

"  "        differential  diagnosis  of 298-300 

'•  "        etiology  of 291 

"  "        morbid  anatomy  of 288-291 

"  "        physical  signs  of 294-297 

"  "        prognosis  of 300 

"  "        symptoms  of 292-294 

"  "        treatment  of 301-305 

chronic,  differential  diagnosis  of 306 

"  "        etiology  of 305 

"  "        morbid  anatomy  of 305 

"        physical  signs  of 305 

"  "        prognosisof 306 

"  "        symptoms  of 305 

"  "        treatment  of 306 

Pericardium,  tuberculosis  of.   ,.,,   .       ...   - .     308 


INDEX.  547 

.  FAGB 

Phthisis,  pulmonary  catarrhal,  morbid  anatomy  of. 215-219 

differential  diagnosis  of . .  .257-2(50 

"          etiology  of. 226 

acquired  feebleness  of  constitution  in  the 228 

anti-hygienic  influences  in  the 228 

climate  in  the 230 

hereditary  predisposition. 227 

mechanical  irritation  of  bronchi 232 

"          fibrous,  morbid  anatomy  of 219-221 

"          physical  signs  of 250-257 

"          prognosis  of. 261-264 

"          stages  of 250 

symptoms  of,  arrest  of  menstruation  as  a 248 

changes  in  the  voice  as  a 248 

clubbing  of  terminal  phalanges  as  a 249 

"  "  cough  as  a. 240 

"  "  diarrhoea  as  a 246 

"  "  disturbed  digestion  as  a 245 

"  dyspnoea  as  a 238 

emaciation  as  a 244 

expectoration  as  a 240 

"  "  "  fever  as  a 242 

haemoptysis  as  a 246 

"  night  sweats  as  a 276 

"  "  "  oedema  of  the  feet  as  a 249 

"  "  "  painasa 239 

"  "  "  pulseasa, 244 

"  "  treatment  of,  climate  in  the 279-283 

"  "  "  cod-liver  oil  in  the 269 

counter-irritants  in  the 275 

"  "  "  diet  in  the 278 

"  "  "  hygienic 277 

hypophosphate  of  lime  in  the 271 

"  "  "  inhalations  in  the 271 

"  "  "  ironinthe 271 

«  "  "  medicinal 267 

"  "  "  opiuminthe 274 

"  "  "  prophylactic 264-297 

"  ««  "  stimulants  in  the 273 

"  "  "  sulphate  of  quinine  in  the 267,277 

"  "  tubercular,  morbid  anatomy  of 221 

"  "  varieties  of 215 

Pleurisy,  acute,  differential  diagnosis  of 197 

"  "      etiology  of 172 

"  "       morbid  anatomy  of 170-172 

"  "       physical  signs  of 174-177 

"  "       prognosis  of *' 

«  "       symptoms  of 172-174 

"  "       treatment  of 178'  179 

"         definition  of •  1| 

"         eubacute,  differential  diagnosis  of 186- 

"  "         etiology  of 1! 

»  »         morbid  anatomy  of 180-182 


548  IXDEX. 

PAGE 

Pleurisy,  subacute,  physical  signs  of 184-186 

"         prognosis  of 188-190 

"         symptoms  of 182-184 

"         treatment  of,  aspirator  in  the 193 

diaphoretics  in  the 190 

"  "  diuretics  in  the 190 

' '  hydragogue  cathartics  in  the 190 

"  iodide  of  iron  in  the 192 

"         varieties  of 169 

Pneumonia,  catarrhal,  acute,  definition  of 151 

"  "  "       differential  diagnosis  of 157 

"  "       etiology  of 154 

'•  "  "       morbid  anatomy  of 151-154 

' '       physical  signs  of 157 

"  "  "       prognosisof 158 

"  "  "       stagesof 152 

"  "  "       symptoms  of 155-157 

"  "       treatment  of,  antiphlogistic 159 

"  "  "  cod-liver  oil  in  the 160 

"  "  "  "  cold  compresses  in  the 160 

"  counter-irritants  in  the 160 

iron  in  the 161 

"  stimulants  in  the 159 

"  "  "  sulphate  of  quinine  in  the 160 

"  "  "  "  temperature  in  the 159 

vapor  inhalations  in  the 160 

croupous,  differential  diagnosis  of 139 

"  "         etiology  of 126 

"  "         morbid  anatomy  of 121-126 

"  "         physical  signs  of 135-139 

"  "         prognosis  of 140-142 

"  "         stages  of 121 

"  "         symptoms  of 128-135 

"  "         treatment  of 143-151 

"  "  "  aconite  in  the 145 

"  "  antimony  in  the 145 

"  "  "  bleeding  in  the 144 

"  "  "  calomelinthe 145 

"  "  cold  compresses  in  the 147 

counter-irritants  in  the 150 

narcotics  in 149 

"  "  stimulants  in  the 141} 

sulphate  of  quinine  in  the 147 

' '  temperature  in  the 146 

41  veratrum  viride  in  the 145 

"  definition  of 120 

"  interstitial,  differential  diagnosis  of 166 

"  "  etiology  of 164 

"  "  morbid  anatomy  of 161-164 

"  "  physical  signs  of 165 

"  "  prognosis  of 167 

"  symptoms  of 164 

11  "  treatment  of...  ,.  167 


INDEX.  549 


PAGE 


Pneumonia,  typhoid 

varieties  of _  120 

Pneumopericardium,  definition  of .  _  307 

diagnosis  of 307 

prognosis  of 307 

Pulmonic  obstruction <  3gQ 

regurgitant,  diagnosis  of . .  361 

prognosis  of 361 

treatment  of 362 

Pyelitis,  definition  of _  ^  530 

differential  diagnosis  of , .  536 

"        etiology  of _  _  593 

morbid  anatomy  of 520 

"        symptoms  of 534,  505 

treatment  of 537 

Pyonephrosis 531 

Thrombosis,  cardiac,  differential  diagnosis  of 420 

"        etiology  of 419 

"        morbid  anatomy  of 418 

"        physical  signs  of 420 

"        prognosis  of 420 

"        symptoms  of 419 

"  "        treatmentof 420 

Tricuspid  regurgitation,  differential  diagnosis  of 367 

"  "  etiology  of 365 

morbid  anatomy  of 364 

physical  signs  of 366 

prognosis  of 368 

symptoms  of 365,  366 

treatment  of 368 

Ursemia,  acute,  convulsions  in 444 

"  coma  in 445 

"  "  differential  diagnosis  of 446,  447 

"  "  etiologyof 442^44 

''  "  prognosis  of 447 

"  "  symptoms  of 444,445 

11  "  treatment  of,  chloroform  in  the 450 

"  "  "  digitalis  in  the 448 

"  "  "  morphine  in  the 450-452 

Whooping-cough,  differential  diagnosis  of 76 

"  "  etiologyof ^ 

'"  "  morbid  anatomy  of ^ 

"  "  physical  signs  of ^ 

"  "  prognosis  of '" 

"  u  symptoms.  (j£ ' 

"  "  treatmentof..              76~78 


Date  Due 


PR.NTED    IN    U.S.*.  CAT.      NO.      24       16! 


A  000  511  629  8 


WF970 
L863L 

1875 
Loomis,  Alfred  L 

Lectures  on  diseases  of  the 
respiratory  organs  . . . 


WF970 
L863L 

1875 
Loomis,  Alfred  L 

Lectures  on  diseases  of  the 
respiratory  organs  . . . 


MEDICAL  SCIENCES  LIBRARY 

UNIVERSITY  OF  CALIFORNIA,  IRVINE 

IRVINE,  CALIFORNIA  92664 


